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IN THE SUPREME COURT OF APPEALS OF WEST VIRGINIA
 

September 2013 Term FILED 

November 13, 2013 

_____________ released at 3:00 p.m. 

RORY L. PERRY II, CLERK 

SUPREME COURT OF APPEALS No. 12-1135 OF WEST VIRGINIA 

DEBORAH KAY HARRIS, ADMINISTRATRIX OF THE ESTATE OF
 

RONALD K. HARRIS, DECEASED,
 

Plaintiff Below, Petitioner
 

V. 

CSX TRANSPORTATION, INC., 

Defendant Below, Respondent 

Appeal from the Circuit Court of Marshall County
 

Honorable David W. Hummel, Judge
 

Civil Action No. 08-C-171M(H)
 

REVERSED AND REMANDED
 

Submitted: October 15, 2013
 

Filed: November 13, 2013
 

R. Dean Hartley James W. Turner 

Julie R. Magers Steptoe & Johnson 

J. Michael Prascik Huntington, West Virginia 

Hartley & O’Brien, P.L.L.C. Andrew E. Tauber 

Wheeling, West Virginia Brian J. Wong 

Attorneys for Petitioner Mayer Brown LLP 

Washington, District of Columbia 

Attorneys for Respondent 

JUSTICE DAVIS delivered the Opinion of the Court. 

CHIEF JUSTICE BENJAMIN concurs and reserves the right to file a concurring 

opinion. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

JUSTICE LOUGHRY dissents and reserves the right to file a dissenting opinion. 

SYLLABUS BY THE COURT 

1. When a circuit court excludes expert testimony as unreliable under the 

Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579, 113 S. Ct. 2786, 125 L. Ed. 2d 

469 (1993), and Wilt v. Buracker, 191 W. Va. 39, 443 S.E.2d 196 (1993), gatekeeper 

analysis, we will review the circuit court’s method of conducting the analysis de novo. 

2. When a trial court is called upon to determine the admissibility of 

scientific expert testimony, in deciding the “reliability” prong of admissibility the focus of 

the trial court’s inquiry is limited to determining whether the expert employed a methodology 

that is recognized in the scientific community for rendering an opinion on the subject under 

consideration. If the methodologyis recognized in the scientific community, the court should 

then determine whether the expert correctly applied the methodology to render his or her 

opinion. If these two factors are satisfied, and the testimony has been found to be relevant, 

and the expert is qualified, the expert may testify at trial. 

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Davis, Justice: 

Deborah Kay Harris, administratrix of the Estate of Ronald K. Harris 

(“Petitioner”), appeals an order of the Circuit Court of Marshall County granting summary 

judgment in favor of CSX Transportation, Inc. (“CSX”). The circuit court granted summary 

judgment after ruling that Petitioner was precluded from calling her three expert witnesses 

at trial. The dispositive issue presented by the Petitioner in this appeal is whether the circuit 

court committed error in finding the scientific testimony of Petitioner’s three expert 

witnesses was not reliable.1 After a careful review of the briefs, the record submitted on 

appeal and listening to the arguments of the parties, we reverse and remand this case. 

I.
 

FACTUAL AND PROCEDURAL HISTORY
 

This action was originally filed by Ronald K. Harris under the Federal 

Employers’ Liability Act2 and the Locomotive Inspection Act3 against his employer, CSX.4 

The complaint alleged that Mr. Harris’ exposure to diesel exhaust fumes while employed by 

1

The Petitioner set out three issues as assignments of error. However, we only 

need to address the issue of the reliability of the testimony of Petitioner’s experts to resolve 

this case. 

2

See 45 U.S.C. §51 et seq. (1939). 

3

See 49 U.S.C. § 0701 et seq. (1994). 

4

The record submitted on appeal did not include the complaint. 

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CSX caused him to develop a type of cancer called multiple myeloma. While the case was 

pending, Mr. Harris died as a result of the cancer. Petitioner, Mr. Harris’ wife and 

administratrix of his estate, was substituted as the plaintiff. Petitioner amended the 

complaint to allege that Mr. Harris’ death resulted from his exposure to diesel exhaust 

fumes.5 

When the parties concluded expert witness discovery, CSX filed a motion to 

exclude the testimony of Petitioner’s three expert witnesses because their methodology was 

not reliable. At the request of CSX, the trial court held an evidentiary hearing regarding the 

admissibility of Petitioner’s expert witnesses’ testimony. The evidentiary hearing lasted two 

days. During the hearing, Petitioner called her three experts, Dr. Peter Infante, Ph.D.; Dr. 

Lawrence Goldstein, Ph.D.; and Dr. Brian Durie, M.D. CSX called two expert witnesses: 

Dr. Peter Shields, M.D. and Dr. Laura Green, Ph.D. These evidentiary hearings in West 

Virginia are commonly referred to as “Daubert/Wilt” hearings. 

At the conclusion of the two-day evidentiary hearing, the circuit court entered 

three orders excluding Petitioner’s experts’ testimony. The circuit court entered findings of 

fact which, in essence, determined that Petitioner failed to prove to the court that diesel 

exhaust exposure causes multiple myeloma. As a result of not having an expert, Petitioner 

5

The amended complaint was not made part of the record on appeal. 

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agreed with CSX to jointly move for summary judgment in CSX’s favor so that Petitioner 

could appeal the adverse expert witness rulings. The circuit court entered an order granting 

summary judgment. This appeal followed. 

II.
 

STANDARD OF REVIEW
 

In this proceeding, the circuit court granted summaryjudgment in favor of CSX 

after excluding the testimony of Petitioner’s expert witnesses. We stated in Syllabus point 

1 of Painter v. Peavy, 192 W. Va. 189, 451 S.E.2d 755 (1994), that “[a] circuit court’s entry 

of summary judgment is reviewed de novo.” The parties agree. Without expert testimony 

by the Petitioner, summary judgment is appropriate. Consequently, the dispositive ruling in 

this case is not the summary judgment order. It is the orders precluding Petitioner’s three 

experts from testifying. If those orders fail, summary judgment is not appropriate. 

As a general matter, we have long held that “[t]he admissibility of testimony 

by an expert witness is a matter within the sound discretion of the trial court, and the trial 

court’s decision will not be reversed unless it is clearly wrong.” Syl. pt. 6, Helmick v. 

Potomac Edison Co., 185 W. Va. 269, 406 S.E.2d 700 (1991). However, we have indicated, 

and so hold, that “when a circuit court excludes expert testimony as unreliable under the 

[Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579, 113 S. Ct. 2786, 125 

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L. Ed. 2d 469 (1993); and Wilt v. Buracker, 191 W. Va. 39, 443 S.E.2d 196 (1993),] 

gatekeeper analysis, we will review the circuit court’s method of conducting the analysis de 

novo.” San Francisco v. Wendy’s Int’l, Inc., 221 W. Va. 734, 740, 656 S.E.2d 485, 491 

(2007) (citations omitted). 

With these standards in mind, we turn to the issues presented by this appeal. 

III.
 

DISCUSSION
 

In order to adequately address the dispositive issue in this case and give 

guidance to trial judges in future cases similar to the instant matter, we have outlined our 

discussion as follows: (1) general principles of Rule 702; (2) the nature of multiple myeloma; 

(3) epidemiological methodology; (4) toxicological methodology; (5) weight of the evidence 

methodology; (6) Bradford Hill methodology; (7) qualification, methodology and opinion of 

the expert witnesses; and (8) the circuit court’s orders excluding the testimony of Petitioner’s 

experts. 

A. General Principles of Rule 702 

Rule 702 of the West Virginia Rules of Evidence provides in full that, “[i]f 

scientific, technical, or other specialized knowledge will assist the trier of fact to understand 

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the evidence or to determine a fact in issue, a witness qualified as an expert by knowledge, 

skill, experience, training, or education may testify thereto in the form of an opinion or 

otherwise.” “Rule 702 reflects an attempt to liberalize the rules governing the admissibility 

of expert testimony.” Weisgram v. Marley Co., 169 F. 3d 514, 523 (8th Cir. 1999). What 

this means is that “[t]he rule ‘is one of admissibility rather than exclusion.’” In re Flood 

Litig. Coal River Watershed, 222 W. Va. 574, 581, 668 S.E.2d 203, 210 (2008) (quoting 

Arcoren v. United States, 929 F.2d 1235, 1239 (8th Cir. 1991). “Disputes as to the strength 

of an expert’s credentials, mere differences in the methodology, or lack of textual authority 

for the opinion go to weight and not to the admissibility of their [sic] testimony.” Gentry v. 

Mangum, 195 W. Va. 512, 527, 466 S.E.2d 171, 186 (1995) (citation omitted). 

The decisions of this Court have “explained that circuit courts must conduct 

a two-part inquiry under Rule 702 and ask: (1) is the witness [qualified as] an expert; and, 

if so, (2) is the expert’s testimony relevant and reliable?” San Francisco v. Wendy’s Int’l, 

Inc., 221 W. Va. at 741, 656 S.E.2d at 492 (citations omitted). See also Robin Jean Davis, 

Admitting Expert Testimony in Federal Courts and Its Impact on West Virginia 

Jurisprudence, 104 W. Va. L. Rev. 485, 513 (2002) (“Trial courts are required to assess 

scientific expert testimony for relevancy and reliability.”). In Syllabus point 5 of Gentry we 

set out the steps that a trial court should take to determine if an expert is qualified to render 

an opinion under Rule 702: 

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In determining who is an expert, a circuit court should 

conduct a two step inquiry. First, a circuit court must determine 

whether the proposed expert (a) meets the minimal educational 

or experiential qualifications (b) in a field that is relevant to the 

subject under investigation (c) which will assist the trier of fact. 

Second, a circuit court must determine that the expert’s area of 

expertise covers the particular opinion as to which the expert 

seeks to testify. 

195 W. Va. 512, 466 S.E.2d 171. 

The general standard for determining whether an expert’s scientific opinion is 

relevant and reliable was set out in Syllabus point 2 of Wilt v. Buracker, 191 W. Va. 39, 443 

S.E.2d 196: 

In analyzing the admissibility of expert testimony under 

Rule 702 of the West Virginia Rules of Evidence, the trial 

court’s initial inquiry must consider whether the testimony is 

based on an assertion or inference derived from the scientific 

methodology. Moreover, the testimony must be relevant to a 

fact at issue. Further assessment should then be made in regard 

to the expert testimony’s reliabilitybyconsidering its underlying 

scientific methodology and reasoning. This includes an 

assessment of (a) whether the scientific theory and its 

conclusion can be and have been tested; (b) whether the 

scientific theory has been subjected to peer review and 

publication; (c) whether the scientific theory’s actual or 

potential rate of error is known; and (d) whether the scientific 

theory is generally accepted within the scientific community. 

As is illustrated later in this opinion, the trial court’s decision to exclude 

Petitioner’s three experts resulted from its determination that the scientific opinions of all 

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three of Petitioner’s experts were not reliable. The circuit court’s ruling shows a 

misunderstanding of the meaning of “reliable” under West Virginia jurisprudence. We 

previously have noted the contours of the meaning of “reliable’” as follows: 

The assessment of whether scientifically-based expert 

testimony is “reliable,” as that term is used in [Daubert v. 

Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579, 113 S. Ct. 

2786, 125 L. Ed. 2d 469 (1993), and Wilt v. Buracker, 191 

W. Va. 39, 443 S.E.2d 196 (1993)], does not mean an 

assessment of whether the testimony is persuasive, convincing, 

or well-founded. Rather, assessing “reliability” is a shorthand 

term of art for assessing whether the testimony is to a reasonable 

degree based on the use of knowledge and procedures that have 

been arrived at using the methods of science—rather than being 

based on irrational and intuitive feelings, guesses, or 

speculation. If the former is the case, then the jury may (or may 

not, in its sole discretion) “rely upon” the testimony. 

In re Flood Litig., 222 W. Va. at 582 n.5, 668 S.E.2d at 211 n.5. 

In Gentry, Justice Cleckley made the following relevant observation: 

Under Daubert/Wilt, the circuit court conducts an inquiry 

into the validity of the underlying science, looking at the 

soundness of the principles or theories and the reliability of the 

process or method as applied in the case. The problem is not to 

decide whether the proffered evidence is right, but whether the 

science is valid enough to be reliable. 

Gentry, 195 W. Va. at 523, 466 S.E.2d at 182 (emphasis in original). It is noteworthy that 

Justice Cleckley felt it was important to italicize the quoted second sentence: “The problem 

is not to decide whether the proffered evidence is right, but whether the science is valid 

enough to be reliable.” Id. As will be shown later in this opinion, the circuit court 

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misapplied this Court’s opinion in Gentry. That is, the circuit court decided the opinions 

from Petitioner’s three experts were wrong. Under Gentry, right or wrong is not an issue of 

the admissibility of scientific evidence. The circuit court made right or wrong a central test 

for the admission of scientific evidence. In doing so, the circuit court removed from the jury 

its exclusive role of deciding which expert opinion to believe. 

Rule 702 and the decisions of this Court clearly state that it is of no moment 

that the opinions of the parties’ experts reach different conclusions on all dispositive issues. 

This is to be expected. Our legal system is adversarial, not cordial. As a result of the 

adversarial essence of our legal system, we rely upon the jury to make the ultimate 

determination as to which expert is right and which expert is wrong. To place the decision 

in the hands of trial judges denies litigants their constitutional right to a jury trial. 

The decision in State ex rel. Wiseman v. Henning, 212 W. Va. 128, 569 S.E.2d 

204 (2002), illustrates this Court’s hostility to stripping litigants of the right to have a jury 

decide if an expert is right or wrong. The plaintiff in Wiseman was injured in an automobile 

accident and later developed multiple myeloma. The plaintiff filed a negligence action 

against the truck driver and truck owner, alleging that his multiple myeloma resulted from 

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a rib cage injury he suffered in the traffic collision with the truck driver.6 The circuit court 

granted defendants’ motion in limine to exclude testimony of the plaintiff’s expert witness 

on causation. The plaintiff filed a petition for a writ of prohibition with this Court seeking 

to prevent enforcement of the trial court’s order. This Court granted the writ after concluding 

that plaintiff’s expert’s proffered opinion was sufficiently reliable to be admissible. The 

opinion in Wiseman addressed the issue as follows: 

Examining the record in the instant case, we believe that 

the circuit court exceeded its authority in its decision to exclude 

the testimony of Dr. Hussein. The record reflects that Dr. 

Hussein was a member of several specialized cancer research 

societies, and had substantial interaction with other cancer 

specialists. He was a specialist in cancers such as that suffered 

by Mr. Wiseman, and was director of the Myeloma Program at 

the Cleveland Clinic. Dr. Hussein’s proffered opinion that 

multiple myeloma can result from a trauma was based upon: his 

extensive treatment of Mr. Wiseman; his treatment of five other 

patients at the Cleveland Clinic who had trauma-induced 

myelomas; his study of the physiological process of tissue injury 

causing chronic inflammation and overstimulation of cells, 

which triggers the growth of cancerous cells; his interaction 

with other specialists who also believe that trauma can trigger 

the occurrence of myeloma; and the handful of published studies 

by other cancer centers that have identified local tissue injury, 

including a bone fracture, as a risk factor for causing multiple 

myeloma. 

We recognize that Dr. Hussein’s opinion is novel and 

unorthodox, and may not have yet received, as the circuit court 

found, “general acceptance in the scientific community.” 

However, the Rules of Evidence do not require that a scientific 

opinion be “generally accepted,” because such a requirement is 

6

A loss of consortium claim was also brought by the plaintiff’s wife. 

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at odds with the liberal thrust of the . . . Rules and their general 

approach of relaxing the traditional barriers to opinion 

testimony. The record suggests a substantial degree of 

reliability underlying the formation of Dr. Hussein’s opinion. 

Accordingly, we find that the circuit court erred in excluding his 

testimony. . . . The proffered opinion is valid enough to be 

reliable; whether the proffered evidence is right is a question for 

the finder of fact. 

Wiseman, 212 W. Va. at 133-34, 569 S.E.2d at 209-10 (internal quotations and citations 

omitted; emphasis added).7 See also Ruiz-Troche v. Pepsi Cola of Puerto Rico Bottling Co., 

161 F.3d 77, 85 (1st Cir. 1998) (“Daubert does not require that a party who proffers expert 

testimony carry the burden of proving to the judge that the expert’s assessment of the 

situation is correct.”). 

B. The Nature of Multiple Myeloma 

In the case sub judice, Mr. Harris was diagnosed with having multiple 

myeloma. He died from this disease. This disease has been described as follows: 

“[M]ultiple myeloma is a cancer of the plasma cell, a cell which 

arises in bone marrow and is an important part of the immune 

system as it provides antibodies which help fight infection and 

other diseases. If a plasma cell becomes malignant, it is called 

a myeloma cell. An individual with myeloma has an abnormal 

build-up of myeloma cells in the bone marrow with 

displacement of normal marrow and which results in tumors that 

involve and destroy surrounding bone. 

7

This opinion will conclude the discussion of the legal principles of 

admissibility of expert testimony in the context of the circuit court’s ruling in Section III G, 

infra. 

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World City Found., Inc. v. Sacchetti, No. 114829/03, 2008 WL 344131, at*4 (N.Y. Sup. Ct. 

Jan. 28, 2008). Specifically, “‘[m]ultiple myeloma’ refers to the presence of numerous 

myelomas in various bones of the body.” Hawaii Med. Serv. Ass’n v. Adams, 209 P.3d 1260, 

1263 n.4 (Haw. Ct. App. 2009). During the underlying proceedings herein, multiple 

Myeloma was described by the expert for CSX, Dr. Shields, as follows: 

So multiple myeloma is a cancer of one of the types of 

blood cells. It’s actually in plasma cells, which is a type of B 

cell, and the plasma cells are responsible for making antibodies 

to fight infection. And what happens is that if you get a 

myeloma, all the plasma cells or one type of plasma cell, 

actually started growing uncontrollably and pushing everything 

out . . . 

. . . . 

. . . So plasma cell is one of the – is one of the blood cells 

that’s part of the immune system that makes those antibodies 

fight, you know, the common cold, pneumonia, that sort of 

thing. 

And so what happens is as those cells grow, those plasma 

cells, and become plasmacytomas; where they like live . . . in 

the bones. And so that’s the myeloma. So the myeloma part is 

the bones, and multiple is you get multiple bone lesions. And as 

it’s – as it’s living in the bones, it starts crowding up the bone 

marrow, and you start having other bood count effects. You 

have immune system problems and that sort of thing. 

See also Toney v. State, 961 N.E.2d 57, 60 (Ind. Ct. App. 2012) (“[M]ultiple myeloma [is] 

a cancer of the plasma cells in bone marrow.”); Williams v. Superior Uniform Grp., Inc., 847 

So. 2d 244, 246 (La. Ct. App. 2003) (“Multiple myeloma is a type of cancer that affects the 

bone marrow, the body’s blood-forming system.”). 

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C. Epidemiological Methodology 

One of Petitioner’s experts, Dr. Infante, is an epidemiologist. Epidemiology 

“refers to the science that studies the distribution of diseases within populations[.]” Chesson 

v. Montgomery Mut. Ins. Co., No. 97, Sept Term, 2012, 2013 WL 5311126, at *17 (Md. Sept. 

24, 2013) (internal quotations and citation omitted). Moreover, 

[e]pidemiology is a methodology. The practice of 

epidemiologyinvolves sampling and matching so as to minimize 

systematic bias and statistical analysis designed to estimate the 

effect of random errors on results. Epidemiology is not a theory 

of how a substance causes cancer, or birth defects, or 

autoimmune disease. These theories come from other 

disciplines. 

4 David L. Faigman et al., Modern Scientific Evidence: The Law and Science of Expert 

Testimony § 35-1.1, at 132 n.18 (2002). “[E]pidemiological studies examine existing 

populations to attempt to determine if there is an association between a disease or condition 

and a factor suspected of causing that disease or condition.” Merrell Dow Pharms. v. 

Havner, 953 S.W.2d 706, 715 (Tex. 1997). The issue of an epidemiological “association” 

has been more fully described as follows: 

[T]he field of epidemiology is not intended to utilize the results 

of a group study to demonstrate causation for any individual 

plaintiff. Instead, the studies are performed or undertaken to 

first determine if a statistically significant association exists 

between an exposure and an outcome. If such an association is 

revealed and the studies are determined to be free of 

confounding, bias, or other error, then an association can be 

established. At this point, epidemiologists and others 

interpreting the epidemiologic data can make an inference 

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vis-à-vis the existence of a causal relationship or the lack 

thereof. 

David C. Woodside, III and Allison G. Davis, The Bradford Hill Criteria: The Forgotten 

Predicate, 35 T. Jefferson L. Rev. 103, 108 (2013). 

It should be clearly understood that the term “association” is a term of art in 

epidemiology. It has been defined as “[t]he degree of statistical dependence between two or 

more events or variables.” In re TMI Litig., 193 F.3d 613, 710 n.159 (3d Cir. 1999) (internal 

quotations and citation omitted). Moreover, an association is not the same as causation. An 

epidemiological association identified in a study may or may not be causal. “Although 

epidemiological studies cannot prove causation, theydo provide a basis for an epidemiologist 

to infer that a chemical agent can cause a disease.” Syl. pt. 7, King v. Burlington Northern 

Santa Fe Ry. Co., 762 N.W.2d 24, 28 (Neb. 2009). “Assessing whether an association is 

causal requires an understanding of the strengths and weaknesses of the study’s design and 

implementation, as well as a judgment about how the study findings fit with other scientific 

knowledge.” Michael D. Green et al., Reference Guide on Epidemiology, in Reference 

Manual on Scientific Evidence 549, 553 (3d ed. 2011). Moreover, the methodological 

soundness of an epidemiological study and its use in resolving causation require answering 

three questions. First, does the study reveal an association between a chemical agent and 

disease? Second, did any errors in the study cause an inaccurate result? Third, is the 

relationship between the chemical agent and the disease causal? See id. at 554. 

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In determining whether an association exists between a suspected chemical 

agent and a disease, epidemiologist primarily rely upon three types of studies: (1) 

experimental studies, (2) cohort studies, and (3) case-control studies.8 See King, 762 N.W.2d 

at 35. Finally, the strength of an association between exposure to a chemical agent and 

disease can be stated as a relative risk, an odds ratio, or an attributable risk. “Each of these 

measurements of association examines the degree to which the risk of disease increases when 

individuals are exposed to an agent.” Green et al., supra, at 566. To better understand this 

epidemiological association, we will review these three main types of studies – experimental 

studies, cohort studies, and case control studies as well as studies that examine the 

association of relative risk, odds ratio, and attributable risk. 

1. Experimental studies. An experimental study has been defined as “a study 

in which a population is selected for a planned trial of a regimen whose effects are measured 

by comparing the outcome of the regime in the experimental group with the outcome of 

another regimen in a control group.” 4 Faigman et al., supra, at 184. This type of study goes 

by several names including, randomized trial, clinical trial, and true experiment. Green et al. 

supra, at 555. 

8

There are also additional types of specialized studies. 

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In order to answer the question of whether a chemical agent is related to a 

certain disease, an epidemiologist may conduct an experimental study in which selected 

participants are randomly assigned to one, of two groups: a group exposed to the chemical 

agent and a group that was not exposed. After a predetermined observation period, the 

participants in both groups are evaluated for the development of the disease. An 

experimental study is often used to evaluate new drugs or medical treatments. Green et al., 

supra, at 555. See also In re Bextra & Celebrex Mktg. Sales Practices & Prod. Liab. Litig., 

524 F. Supp. 2d 1166 (N.D. Cal. 2007) (wherein a clinical study that revealed Celebrex 

increased cardiovascular risk was relied upon by the court to conclude that the plaintiff’s 

experts’ testimony on causation was admissible); McDarby v. Merck & Co., 949 A.2d 223 

(N.J. Super. Ct. App. Div. 2008) (explaining how clinical trials of Vioxx revealed an 

association with heart disease). 

Of course, if a chemical agent’s effects are harmful, a researcher cannot 

knowingly expose participants to the chemical. In situations where the chemical agent is 

harmful, a researcher will typically “observe” selected participants who have already been 

exposed to the chemical, e.g., comparing those already exposed to an industrial chemical 

agent with another group of participants who have not been exposed. In this situation, the 

researcher compares the rate of disease or death of the exposed group with that of an 

unexposed group. Green et al., supra, at 555-56. 

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2. Cohort studies. A cohort study has been defined as an “analytical method 

of epidemiologic study in which subsets of a defined population can be identified who . . . 

have been . . . exposed . . . to a factor . . . hypothesized to influence the probability of 

occurrence of a given disease[.]” Faigman et al., supra, at 183. A cohort study is also called 

a prospective study and followup study. Green et al., supra, at 557. 

A cohort study involves the use of a study population without regard to the 

disease status of the participants. A researcher may define a study population in the present 

and follow it into the future, or design a study population retrospectively at a point in the past 

and follow it over historical time toward the present. In either situation, the researcher will 

classify the study population into groups based on whether the group members were exposed 

to the chemical agent of interest. The task of a researcher in a retrospective population study 

is to determine the number of people in the exposed group who developed the disease of 

interest, from all available reliable sources, and compare that number of people with the 

number of people of the group who were not exposed. With respect to a prospective study, 

the exposed and unexposed populations are followed for a predetermined length of time, and 

the number of persons in each group who develop the disease of interest are compared. 

Green et al., supra, at 557. See also Faigman et al., supra, at 162-65. 

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A cohort studyhas the advantage of allowing the temporal relationship between 

exposure and disease to be established more quickly than in other study design. As a result 

of following a study population that is not initially affected by the disease, the researcher is 

able to determine the exact onset time of the disease and its relation to exposure to the 

chemical. For a researcher, “[t]his temporal relationship is critical to the question of 

causation, because exposure must precede disease onset if exposure caused the disease.” 

Green et al, supra, at 558. 

3. Case control studies. A case control study involves selecting a group of 

individuals who have a disease of interest (cases), and choosing a similar group of persons 

who do not have the disease of interest (controls). When the groups are selected, the 

researcher will then compare them in terms of past exposures. In doing so, the researcher is 

seeking to determine whether a certain exposure that is associated with the disease resulted 

in a higher proportion of past exposure among the “cases” than among the “controls”. 

“[C]ase-control studies are . . . particularly useful in the study of rare diseases, because if a 

cohort study were conducted, an extremely large group would have to be studied in order to 

observe the development of a sufficient number of cases for analysis.” Green et al., supra, 

at 559. See also 4 Faigman et al., supra, at 166-69. 

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4. Relative risk. The strength of an association between exposure to a 

chemical agent and disease can be stated as a relative risk. This concept of “relative risk” 

is defined as the ratio of the incidence rate of a targeted disease in an exposed population to 

the incidence rate in an unexposed population. Additionally, the “incidence rate of a targeted 

disease” is defined as the total number of cases of the disease that manifests itself during a 

predetermined time period divided by the number of individuals in the population being 

studied. In sum, the incidence rate illustrates the risk that an individual in a population group 

will develop the targeted disease within a predetermined time period. Green et al., supra, at 

566-67. 

For example, assume that a group composed of 100 individuals is exposed to 

a chemical agent, and a group composed of 200 individuals is not exposed to the chemical. 

After a researcher studies both groups for one year, it is learned that 40 of the individuals 

exposed to the chemical have the targeted disease, and 20 of the individuals who were not 

exposed to the chemical are also found to have the disease. The relative risk of contracting 

the disease would be determined as follows: 

[1] The incidence rate of disease in the exposed individuals is 40 

cases per year per 100 persons (40/100), or 0.4. 

[2] The incidence rate of disease in the unexposed individuals 

is 20 cases per year per 200 persons (20/200), or 0.1. 

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[3] The relative risk is calculated as the incidence rate in the 

exposed group (0.4) divided by the incidence rate in the 

unexposed group (0.1), or 4.0. 

Green et al., supra, at 567. As a general matter, the relative risk is interpreted as follows: 

[1] If the relative risk equals 1.0, the risk in exposed individuals 

is the same as the risk in unexposed individuals. There is no 

association between exposure to the agent and disease. 

[2] If the relative risk is greater than 1.0, the risk in exposed 

individuals is greater than the risk in unexposed individuals. 

There is a positive association between exposure to the agent 

and the disease, which could be causal. 

[3] If the relative risk is less than 1.0, the risk in exposed 

individuals is less than the risk in unexposed individuals. There 

is a negative association, which could reflect a protective or 

curative effect of the agent on risk of disease. . . . 

Green et al., supra, at 566-67. See also Daniel J. Brown, Clear as Mud – The Role of 

Epidemiological Data in Assessing Admissibility under Delaware Rule of Evidence 702, 13 

Del. L. Rev. 71, 79 (2012) (“The size of the relative risk indicates the strength of that 

association. For example, a relative risk of 3.5 means the risk of disease in those exposed 

to the substance is three and half times higher than the risk of disease in those who were not 

exposed.”). 

5. Odds ratio. The odds ratio, like the relative risk, is used to illustrate in 

quantitative terms the association between exposure to a chemical agent and a disease. This 

tool is considered an easy way to estimate the risk in a case-control study when a rare disease 

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is under investigation.9 The odds ratio permits an approximation of the risk when a rare 

disease is the focus of the study. The odds ratio, in a case-control study, is the ratio of the 

odds that a case group (one with the disease) was exposed to a chemical agent to the odds 

that a control group (one without the disease) was exposed to the same chemical. However, 

in a cohort study, the odds ratio is expressed as the ratio of the odds of developing a disease 

when exposed to a chemical to the odds of developing the disease when not exposed to the 

chemical. Green et al., supra, at 568. 

For example, a researcher conducts a case-control study that has 100 

individuals with a disease who act as the “case” group, and 100 individuals who do not have 

the disease act who were the “control” group. It is found that 40 of the 100 case group 

individuals were exposed to a chemical agent, and 60 were not. In the control group, 20 

9

It has been noted that 

[a] relative risk cannot be calculated for a case-control 

study, because a case-control study begins by examining a group 

of persons who already have the disease. That aspect of the 

study design prevents a researcher from determining the rate at 

which individuals develop the disease. Without a rate or 

incidence of disease, a researcher cannot calculate a relative 

risk. 

Green et al., Reference Guide on Epidemiology, in Reference Manual on Scientific Evidence 

549, 568 n.58 (3d ed. 2011). 

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individuals were exposed to the chemical, and 80 were not. The calculation of the odds ratio 

would be as follows: 

(40/60)
 

OR = ——— = 2.67
 

(20/80)
 

Green et al., supra, at 569. 

[B]ecause an odds ratio approximates the relative risk, the same 

general rules of interpretation apply, i.e., an odds ratio of 1.0 

indicates that there is no association between exposure and 

disease, whereas an odds ratio above 1.0 indicates a positive 

association and an odds ratio below 1.0 indicates a negative 

association. 

Brown, supra, 13 Del. L. Rev. at 79. 

6. Attributable risk. Another epidemiological measurement of risk is called 

attributable risk. This measurement tool represents the amount of disease that individuals are 

exposed to that may be attributed to such exposure. Attributable risk also can be formulated 

as the proportion of the disease among exposed individuals that is linked to the exposure. 

“[T]he attributable risk reflects the maximum proportion of the disease that can be attributed 

to exposure to an agent and consequently the maximum proportion of disease that could be 

potentially prevented by blocking the effect of the exposure or by eliminating the exposure.” 

Green et al., supra, at 570. Stated differently, if the epidemiological association of the 

disease and chemical agent is causal, “the attributable risk is the proportion of disease in an 

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exposed population that might be caused by the agent and that might be prevented by 

eliminating exposure to that agent.” Id. 

The following example has been given to illustrate the determination of 

attributable risk: 

For example, if the incidence rate in the unexposed group 

is ten and the incidence rate in the exposed is fifty then the 

attributable risk is 80 percent (i.e., 50-10 = 40; 40/50 = 80%). 

This would mean that 80 percent of the disease in the exposed 

group is attributable to the exposure to the suspect substance. 

This, however, is not the same as stating that 80 percent of the 

disease is caused by the exposure. 

Brown, supra, 13 Del. L. Rev. at 80. 

D. Toxicological Methodology 

Another of the Petitioner’s experts, Dr. Goldstein, is a toxicologist. The record 

also shows that one of the experts called by CSX, Dr. Green, is likewise a toxicologist. 

“[T]he science of toxicology can help understand whether the dose of a substance achieved 

following a particular exposure has any relationship to toxicity or disease.” David L. Eaton, 

Scientific Judgment and Toxic Torts–Primer in Toxicology for Judges and Lawyers, 12 J.L. 

& Pol’y 5, 12 (2003). Toxicology is a science that focuses on understanding and identifying 

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the harmful effects of chemical agents.10 Toxicological studies alone do not purport to 

provide direct evidence a disease was caused by a chemical exposure. This discipline can, 

however, be instrumental in offering scientific data regarding the increased risk of 

contracting a disease based upon dosage. Bernard D. Goldstein and Mary Sue Henifin, 

Reference Guide on Toxicology, in Reference Manual on Scientific Evidence 633, 635-37 

(3d ed. 2011). Courts have held that toxicologists can provide expert testimony on whether 

a chemical agent caused a disease. See Bonner v. ISP Techs., Inc., 259 F.3d 924, 928-31 (8th 

Cir. 2001); Loudermill v. Dow Chem. Co., 863 F.2d 566, 569–70 (8th Cir. 1988).11 

10“The discipline of toxicology is based primarily upon the sciences of 

chemistry and biology.” 4 Faigman et al., Modern Scientific Evidence: The Law and Science 

of Expert Testimony § 35-1-1, at 104 (2002). 

11One commentator summarized the science of toxicology as follows: 

There are three basic tenets of toxicology: (1) all 

chemicals have the potential to be harmful given the right 

dosage; (2) many chemical agents have a signature pattern of 

toxic effects that are used to establish causation; and (3) 

responses in laboratory animals are useful in determining the 

potential effects on humans. Toxicology generally seeks to 

identify chemicals that pose a threat to human populations and 

the risks associated with a chemical exposure at a given dose. 

Unlike epidemiology, which seeks primarily to establish 

causation, toxicology seeks primarily to estimate the given risks 

associated with potential exposure. 

Carl H. Johnson, When Science Is Too Daunting: Multiple Chemical Sensitivity, Federal 

Courts, and the Struggling Spirit of Daubert, 1 Vill. Envtl. L.J. 273, 291-92 (2000). See also 

4 Faigman et al., supra note 10, at 107. 

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639.14 

“[D]ata from properly designed and evaluated studies in experimental animals 

have been and continue to be reliable sources of information for the identification of 

potential human health hazards and the estimation of risks in exposed populations.” Ronald 

L. Melnick and John R. Bucher, Determining Disease Causality From Experimental 

Toxicology Studies, 15 J.L. & Pol’y 113, 133 (2007). See also 4 Faigman et al., supra, at 109 

(“There is an overwhelming biological similarity between humans and other animals, 

particularly mammals.”). The general testing procedure used by toxicologists involves 

exposing laboratory animals12 or cells/tissues13 to a chemical agent, monitoring changes, and 

comparing those changes with those for an unexposed control group. Of course, there is an 

ongoing debate as to the extent to which animal testing will validly reflect human responses 

to a chemical agent. This debate, however, is circular because it is unethical and potentially 

criminal to experiment on humans by exposing them to hazardous doses of a chemical agent. 

Thus, animal toxicological studies provide the best readily accessible scientific data 

concerning the risk of disease from a chemical exposure. Goldstein and Henifin, supra, at 

12This is called in vivo research. 

13This is called in vitro research. 

14The justification and reliability of animal studies for the potential effects of 

chemicals on humans has been stated as follows: 

Why are animal models used to evaluate human risk? 

The most obvious explanation is that it is unethical to test for 

(continued...) 

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A central component of a toxicological study will involve dose-response 

relationships. 4 Faigman, supra, at 107-08. That is, experiments with animals are conducted 

to determine the dose-response relationship of a chemical agent by measuring how the 

response varies with different doses. Information obtained from this technique “is useful in 

understanding the mechanisms of toxicity and extrapolating data from animals to humans.” 

Goldstein and Henifin, supra, at 641. In making a causation opinion about a chemical and 

a disease, a toxicologist will consider the extent of a person’s dose exposure. Goldstein and 

Henifin, supra, at 638.15 

14(...continued) 

adverse health effects, such as cancer, in humans through 

intentional exposures. Just as animal models are used in 

preclinical trials of new pharmaceutical agents before testing in 

humans, experimental studies performed on animals have been 

used to assess potential health risks of toxic and carcinogenic 

agents in our workplace and general environment. The 

predictive value of animal studies is based on species 

similarities in the biological processes of disease induction. 

Another major advantage of animal studies is the elimination of 

the need to wait for a high incidence of human cancers, which 

may take as much as 30 years from time of first exposure to 

clinical manifestation of disease, before implementing public 

health protective strategies. 

Melnick and Bucher, Determining Disease Causality From Experimental Toxicology Studies, 

15 J.L. & Pol’y 113, at 115-16 (2007). 

15The following is an explanation and illustration of dose: 

Dose is a function of both concentration and duration. 

Haber’s rule is a century-old simplified expression of dose 

effects in which the effect of a concentration and duration of 

(continued...) 

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The approach taken by toxicologists for assessing exposure to a harmful 

chemical agent has been summarized as follows: 

Exposure assessment methodologies include mathematical 

models predicting exposure resulting from an emission source, 

which might be a long distance upwind; chemical or physical 

measurements of media such as air, food, and water; and 

biological monitoring within humans, including measurements 

of blood and urine specimens. An exposure assessment should 

also look for competing exposures. In this continuum of 

exposure metrics, the closer to the human body, the greater the 

overlap with toxicology. 

Goldstein and Henifin, supra, at 657. 

15(...continued) 

exposure is a constant (e.g., exposure to an agent at 10 parts per 

million for 1 hour has the same impact as exposure to 1 part per 

million for 10 hours). Exposure levels, which are concentrations, 

are often confused with dose. This can be particularly 

problematic when attempting to understand the implications of 

exposure to a level that exceeds a regulatory standard that is set 

for a different time frame. For example, assume a drinking water 

contaminant is a known cause of cancer. To avoid a 1 in 

100,000 lifetime risk caused by this contaminant in drinking 

water, and assuming that the average person will drink 

approximately 2000 mL of water daily for a lifetime, the 

regulatory authority sets the allowable contaminant standard in 

drinking water at 10 μg/L. Drinking one glass of water 

containing 20 μg/L of this contaminant, although exceeding the 

standard, does not come close to achieving a “reasonably 

medically probable” cause of an individual case of cancer. 

Goldstein and Henifin, Reference Guide on Toxicology, in Reference Manual on Scientific 

Evidence 633, 638 n.12 (3d ed. 2011). 

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A toxicologist’s opinion on causation should be based upon three preliminary 

assessments: 

First, the expert should analyze whether the disease can 

be related to chemical exposure by a biologically plausible 

theory. Second, the expert should examine whether the plaintiff 

was exposed to the chemical in a manner that can lead to 

absorption into the body. Third, the expert should offer an 

opinion about whether the dose to which the plaintiff was 

exposed is sufficient to cause the disease. 

Goldstein and Henifin, supra, at 661. See also Eaton, supra, 12 J.L. & Pol’y at 38-40; 

Robert C. James, Role of Toxicology in Toxic Tort Litigation: Establishing Causation, 61 

Def. Couns. J. 28, 29 (1994). Courts also have recognized a “three-step methodology for 

toxicologists endorsed by the World Health Organization[.]” Young v. Burton, 567 

F. Supp. 2d 121, 129 (D.D.C. 2008). The risk assessment methodology has been described 

as follows: 

First, an evaluation is made of the chemicals to which the 

individual might have been exposed, and of the concentrations 

of these chemicals in air breathed by the individual. The second 

step involves an evaluation, based on the published scientific 

literature, of the exposures necessary to produce the adverse 

effects associated with the chemicals to which individuals may 

be exposed. These two evaluations are then combined in the 

final step of the risk assessment to provide an estimate of the 

likelihood that any of the harmful properties of any or all of the 

chemicals might have been expressed in the exposed individual. 

Bombardiere v. Schlumberger Tech. Corp., 934 F. Supp. 2d 843, 848-49 (N.D. W. Va. 2013). 

See also Evans v. Toyota Motor Corp., No. V-03-09, 2005 WL 3454456, at*4 (S.D. Tex. 

Aug. 9, 2005); Roche v. Lincoln Prop. Co., 278 F. Supp. 2d 744, 754 (E.D. Va. 2003); 

27
 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Mancuso v. Consolidated Edison Co. of New York, Inc., 967 F. Supp. 1437, 1445 (S.D.N.Y. 

1997); Cavallo v. Star Enter., 892 F. Supp. 756, 764 (E.D. Va. 1995), aff’d, in part, and 

rev’d, in part, 100 F.3d 1150 (4th Cir. 1996); Craig T. Smith, Peering into the Microscope: 

The Rise of Judicial Gatekeeping after Daubert and its Effect on Federal Toxic Tort 

Litigation, 13 B.U. J. Sci. & Tech. L. 218, 227 (2007); Neal C. Stout and Peter A. Valberg, 

Bayes’ Law, Sequential Uncertainties, and Evidence of Causation in Toxic Tort Cases, 38 

U. Mich. J.L. Reform 781, 900 (2005). 

E. Weight of the Evidence Methodology 

One of the Petitioner’s experts, toxicologist Dr. Goldstein, indicated during his 

testimony that he relied upon the weight of the evidence methodology in rendering his 

opinion.16 “[T]he term ‘weight of evidence’ is used to characterize a process or method in 

which all scientific evidence that is relevant to the status of a causal hypothesis is taken into 

account.” Sheldon Krimsky, The Weight of Scientific Evidence in Policy and Law, 95 Am. 

J. Pub. Health S129 (2005). Under this approach, an “expert considers all available studies 

and determines the weight to be afforded to each on the basis of the strengths and weaknesses 

of the individual studies.” Thomas O. McGarity and Sidney A. Shapiro, Regulatory Science 

16It was previously indicated that CSX’s expert, Dr. Green, is a toxicologist. 

However, her testimony was far too acrimonious and rambling to clearly understand what 

precise methodology she used. 

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in Rulemaking and Tort: Unifying the Weight of the Evidence Approach, 3 Wake Forest J.L. 

& Pol’y 65, 78 (2013). 

The phrase “weight of the evidence” is often accorded different meanings by 

scientists. As explained by one court: 

The weight of evidence method [WOE] is used in 

medical literature either in a rigorous scientific or metaphorical 

sense. It is used as methodology where WOE points to 

established interpretative methodologies (e.g., systematic 

narrative review, meta-analysis, causal criteria, and/or quality 

criteria for toxicological studies). . . . The metaphorical use of 

the term is, if nothing else, a colorful way to say the body of 

evidence we have examined and judged using a method we have 

not described but could be more or less inferred from a careful 

between-the-lines reading of our paper. 

Reeps ex rel. Reeps v. BMW of N. Am., LLC, No. 100725/08, 2013 WL 2362566, at *3 

(N.Y. Sup. Ct., May 10, 2013) (internal quotations and citations omitted)).17 The weight of 

17The different ways in which weight of the evidence may be used by scientists 

have been summarized as follows: 

WOE has several distinct uses in contemporary scientific 

practice. First, it most often appears in a metaphorical sense, 

pointing to a body of scientific evidence without reference to 

any specific methodology. . . . Second, in some situations, a 

WOE approach specifically refers to a technique in which “all 

available evidence” should be examined and interpreted. . . . 

Third, often a WOE method refers directly to some other 

synthetic method, such as the systematic narrative review, 

meta-analysis, or the so-called “causal criteria” associated most 

often with the public health discipline of epidemiology. Fourth, 

(continued...) 

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the evidence methodology is used by regulatory agencies such as the Environmental 

Protection Agency18 and the Occupational Safety and Health Administration. “Regulatory 

agencies or risk analysis panels use [the weight of evidence method] to assess the total value 

of the scientific evidence that a substance may be dangerous to human health.” Krimsky, 

17(...continued) 

a WOE method may point to an institutional approach to 

synthesis. . . . Finally, in relatively rare instances of health-risk 

assessment, a WOE approach involves a method that assigns 

numerical weights to individual scientific studies and creates 

summary numeric assessments using mathematical algorithms. 

Douglas L. Weed, Evidence Synthesis and General Causation: Key Methods and an 

Assessment of Reliability, 54 Drake L. Rev. 639, 639 (2006). 

18In the EPA’s 2005 “Guidelines for Carcinogen Risk Assessment” it described 

the type of data that would be considered in its weight of the evidence methodology: 

1.3.3. Weight of Evidence Narrative 

The cancer guidelines emphasize the importance of 

weighing all of the evidence in reaching conclusions about the 

human carcinogenic potential of agents. This is accomplished in 

a single integrative step after assessing all of the individual lines 

of evidence. . . . Evidence considered includes tumor findings, 

or lack thereof, in humans and laboratory animals; an agent’s 

chemical and physical properties; its structure-activity 

relationships (SARs) as compared with other carcinogenic 

agents; and studies addressing potential carcinogenic processes 

and mode(s) of action, either in vivo or in vitro. Data from 

epidemiologic studies are generally preferred for characterizing 

human cancer hazard and risk. 

U.S. Environmental Protection Agency, Guidelines for Carcinogen Risk Assessment 1-11 

(2005), http://www.epa.gov/ttn/atw/cancer_guidelines_final_3-25-05.pdf (last visited on 

Nov. 8, 2013). 

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supra, at S139. See also King, 762 N.W.2d at 39-40 (“[G]overnment agencies and some 

experts use a weight-of-the-evidence methodology. That methodology comprehensively 

analyzes the data from different scientific fields, primarily animal tests and epidemiological 

studies, to assess carcinogenic risks.”). In commenting upon the weight of the evidence 

methodology, Justice Stevens noted the following: 

[T]he Court of Appeals expressly decided that a “weight of the 

evidence” methodology was scientifically acceptable. To this 

extent, the Court of Appeals’ opinion is persuasive. It is not 

intrinsically “unscientific” for experienced professionals to 

arrive at a conclusion by weighing all available scientific 

evidence—this is not the sort of “junk science” with which 

Daubert was concerned. 

General Elec. Co. v. Joiner, 522 U.S. 136, 153, 118 S. Ct. 512, 522-23, 139 L. Ed. 2d 508 

(1997) (Stevens, J., concurring, in part, and dissenting, in part). 

The court in Milward v. Acuity Specialty Products Group, Inc., 639 F.3d 11 

(1st Cir. 2011), explained the weight of the evidence methodology as follows: 

This “weight of the evidence” approach to making causal 

determinations involves a mode of logical reasoning often 

described as “inference to the best explanation,” in which the 

conclusion is not guaranteed by the premises. . . . [I]nference to 

the best explanation can be thought of as involving six general 

steps, some of which may be implicit. The scientist must (1) 

identify an association between an exposure and a disease, (2) 

consider a range of plausible explanations for the association, 

(3) rank the rival explanations according to their plausibility, (4) 

seek additional evidence to separate the more plausible from the 

less plausible explanations, (5) consider all of the relevant 

available evidence, and (6) integrate the evidence using 

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professional judgment to come to a conclusion about the best 

explanation. 

. . . . 

The fact that the role of judgment in the weight of the 

evidence approach is more readily apparent than it is in other 

methodologies does not mean that the approach is any less 

scientific. No matter what methodology is used, an evaluation 

of data and scientific evidence to determine whether an 

inference of causation is appropriate requires judgment and 

interpretation. The use of judgment in the weight of the 

evidence methodologyis similar to that in differential diagnosis, 

which we have repeatedly found to be a reliable method of 

medical diagnosis. 

Milward, 639 F.3d at 17-18 (internal quotations and citations omitted). See also Thomas O. 

McGarity and Sidney A. Shapiro, Regulatory Science in Rulemaking and Tort: Unifying the 

Weight of the Evidence Approach, 3 Wake Forest J.L. & Pol’y 65, 97 (2013) (“Both common 

law courts and regulatory agencies should consider expert opinion based on weight of the 

evidence evaluations of the available scientific information in accordance with valid 

scientific criteria, such as the Bradford Hill criteria, for evaluating evidence.”); Kimberly 

Gordy, The 9/11 Cancer Conundrum: The Law, Policy, & Politics of the Zadroga Act, 37 

Seton Hall Legis. J. 33, 83 (2012) (“The Milward court . . . provides useful guidance for 

weighing evidence. . . . It endorsed the ‘weight of the evidence’ approach, which 

encompasses the Bradford Hill methodology.”). 

F. Bradford Hill Methodology 

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Petitioner’s experts, Dr. Durie and Dr. Infante, relied upon the Bradford Hill 

methodology in rendering their opinions. The record also showed that the expert for CSX, 

Dr. Shield, relied upon the Bradford Hill Methodology. This methodology involves the use 

of criteria set out by epidemiologist Sir Austin Bradford Hill in an article he published in 

1965. See Sir Austin Bradford Hill, The Environment and Disease: Association or 

Causation?, 58 Proc. Royal Soc’y Med. 295 (1965). The Bradford Hill criteria, as they are 

called,19 are “considered relevant for determining whether an epidemiologically-observed 

correlation between a potential causal agent and a disease can or cannot legitimately be 

treated as a cause rather than as merely an association.” Jennifer L. Mnookin, Atomism, 

Holism, and the Judicial Assessment of Evidence, 60 UCLA L. Rev. 1524, 1524 (2013). 

Stated differently, the Bradford Hill criteria are factors that are considered when a researcher 

seeks to determine whether an observed epidemiological association between a disease and 

a chemical agent is causal. Nonnon v. City of New York, 932 N.Y.S.2d 428, 433 (2011). See 

also Gannon v. United States, 571 F. Supp. 2d 615, 624 (E.D. Pa. 2007) (“Other preeminent 

scientists have relied on and adapted the Bradford Hill criteria to determine whether a virus 

can be deemed to cause human cancer.”). “[C]ourts that have considered the question have 

held that it is not proper methodology for an epidemiologist to apply the Bradford Hill factors 

19They are also known as the Bradford Hill viewpoints. See Magistrini v. One 

Hour Martinizing Dry Cleaning, 180 F. Supp. 2d 584, 592 n.9 (D.N.J. 2002) (“These factors, 

first set forth by Sir Austin Bradford Hill, also have been referred to as ‘viewpoints’[.]”). 

33
 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

without data from controlled studies showing an association.” In re Fosamax Prods. Liab. 

Litig., 645 F. Supp. 2d 164, 188 (S.D.N.Y. 2009). 

The Bradford Hill criteria include: (1) strength of the association, (2) 

consistency of the association, (3) specificity of the association, (4) temporal relationship of 

the association, (5) biological gradient or dose-response curve of the association, (6) 

plausibility of the causation, (7) coherence of the explanation, (8) experimental data, and (9) 

existence of analogous causal relationships. Hill, supra, 58 Proc. Royal Soc’y Med. at 295­

99. See also Watson v. Dillon Cos., Inc., 797 F. Supp. 2d 1138, 1150 (D. Colo. 2011); 

Merrell Dow Pharms., Inc. v. Havner, 953 S.W.2d 706, 718-19 (Tex. 1997).20 

The Bradford Hill criteria are “not exhaustive and that no one type of evidence 

must be present before causality may be inferred.” Milward, 639 F.3d at 17. See also In re 

Asbestos Litig., 900 A.2d 120, 134-35 (Del. Super. Ct. 2006) (“None of these criteria stand 

alone; they are all important when considering the issues of association and risk.”). That is, 

“one or more of the factors may be absent even where a causal relationship exists[.]” 

20The “weight of the evidence” methodology can be used along with the 

Bradford Hill criteria. See Milward, 639 F.3d at 17. 

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Magistrini v. One Hour Martinizing Dry Cleaning, 180 F. Supp. 2d 584, 592 n.9 (D.N.J. 

2002).21 Comments on each of the Bradford Hill criteria follow. 

1. Strength of association. Showing that a strong association exists between 

a chemical agent and a disease is more likely indicative of a causal relationship. That is, the 

stronger the relationship between the chemical agent and the disease, the less likely it is that 

the relationship is due to chance or an extraneous variable (a confounder). Hill provided the 

following example of this criterion: 

To take a more modern and more general example upon 

which I have now reflected for over fifteen years, prospective 

inquiries into smoking have shown that the death rate from 

cancer of the lung in cigarette smokers is nine to ten times the 

rate in non-smokers and the rate in heavy cigarette smokers is 

twenty to thirty times as great. On the other hand the death rate 

from coronary thrombosis in smokers is no more than twice, 

possibly less, the death rate in nonsmokers. Though there is 

good evidence to support causation it is surely much easier in 

21This point also was emphasized by Hill, who cautioned in his article: 

None of my nine viewpoints can bring indisputable 

evidence for or against the cause and effect hypothesis and none 

can be required as a sine qua non. What they can do, with 

greater or less strength, is to help us to make up our minds on 

the fundamental question-is there any other way of explaining 

the set of facts before us, is there any other answer equally, or 

more, likely than cause and effect? 

Sir Austin Bradford Hill, The Environment and Disease: Association or Causation? , 58 

Proc. Royal Soc’y Med. 295, 299 (1965). 

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this case to think of some features of life that may go 

hand-in-hand with smoking – features that might conceivablybe 

the real underlying cause or, at the least, an important 

contributor, whether it be lack of exercise, nature of diet or other 

factors. But to explain the pronounced excess in cancer of the 

lung in any other environmental terms requires some feature of 

life so intimately linked with cigarette smoking and with the 

amount of smoking that such a feature should be easily 

detectable. 

Hill, supra, 58 Proc. Royal Soc’y Med. at 295-96. See also King, 762 N.W.2d at 40 

(“[R]egarding an association’s strength, the higher the relative risk, the greater the likelihood 

that a relationship is causal. Yet lower relative risks can reflect causality.”). 

2. Consistency of the association. The consistency of association criterion 

seeks to determine whether a similar association may be found in a variety of different 

situations. Showing numerous observations of an association, with different people in 

diverse situations with different measurement tools, will increase the credibility of an 

association finding. Hill provided the following commentary on this factor: 

This requirement may be of special importance for those 

rare hazards singled out in the Section’s terms of reference. 

With many alert minds at work in industry today many an 

environmental association may be thrown up. Some of them on 

the customary tests of statistical significance will appear to be 

unlikely to be due to chance. Nevertheless whether chance is 

the explanation or whether a true hazard has been revealed may 

sometimes be answered onlybya repetition of the circumstances 

and the observations. 

Returning to my more general example, the Advisory 

Committee to the Surgeon-General of the United States Public 

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Health Service found the association of smoking with cancer of 

the lung in 29 retrospective and 7 prospective inquiries. The 

lesson here is that broadly the same answer has been reached in 

quite a wide variety of situations and techniques. In other words 

we can justifiably infer that the association is not due to some 

constant error or fallacy that permeates every inquiry. And we 

have indeed to be on our guard against that. 

Hill, supra, 58 Proc. Royal Soc’y Med. at 296. See also Frank C. Woodside, III and Allison 

G. Davis, The Bradford Hill Criteria: The Forgotten Predicate, 35 T. Jefferson L. Rev. 103, 

116 (2013) (“Reduced to an elementary level, consistency demonstrates that the results of a 

particular study are not an outlier result. Consistency indicates that the results are generally 

concurrent with the results of other studies–not that they are generally accepted.”). 

3. Specificity of the association. The specificity factor seeks to show that an 

effect, e.g., lung cancer, has only one cause, smoking. Hill discussed this factor as follows: 

If, as here, the association is limited to specific workers 

and to particular sites and types of disease and there is no 

association between the work and other modes of dying, then 

clearly that is a strong argument in favour of causation. 

. . . . 

Coming to modern times the prospective investigations 

of smoking and cancer of the lung have been criticized for not 

showing specificity - in other words the death rate of smokers is 

higher than the death rate of non-smokers from many causes of 

death. But here surely one must return to my first characteristic, 

the strength of the association. If other causes of death are raised 

10, 20 or even 50% in smokers whereas cancer of the lung is 

raised 900-1,000% we have specificity–a specificity in the 

magnitude of the association. 

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We must also keep in mind that diseases may have more 

than one cause. It has always been possible to acquire a cancer 

of the scrotum without sweeping chimneys or taking to 

mulespinning in Lancashire. One-to-one relationships are not 

frequent. Indeed I believe that multicausation is generally more 

likely than single causation though possibly if we knew all the 

answers we might get back to a single factor. 

In short, if specificity exists we may be able to draw 

conclusions without hesitation; if it is not apparent, we are not 

thereby necessarily left sitting irresolutely on the fence. 

Hill, supra, 58 Proc. Royal Soc’y Med. at 297. See also Woodside and Davis, supra, 35 T. 

Jefferson L. Rev. at 116 (“The crux of the specificity consideration is that causation is likely 

if a very specific population at a specific site develops a disease with no other likely 

explanation. More specifically, well performed studies demonstrating an association 

between a specific exposure and a clearly defined disease or condition–otherwise known as 

the case definition–are of more value in inferring the existence of a causal relationship than 

studies with poorly defined exposures and/or loosely defined diseases or conditions.”). 

4. Temporal relationship of the association. This factor seeks to assure that 

the exposure to a chemical agent preceded the disease by a reasonable amount of time, i.e., 

a cause must precede an effect in time. Hill commented briefly on this factor as follows: 

My fourth characteristic is the temporal relationship of 

the association–which is the cart and which the horse? This is a 

question which might be particularly relevant with diseases of 

slow development. Does a particular diet lead to disease or do 

the early stages of the disease lead to those peculiar dietetic 

habits? Does a particular occupation or occupational 

environment promote infection by the tubercle bacillus or are 

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the men and women who select that kind of work more liable to 

contract tuberculosis whatever the environment–or, indeed, have 

they already contracted it? This temporal problem may not arise 

often but it certainly needs to be remembered, particularly with 

selective factors at work in industry. 

Hill, supra, 58 Proc. Royal Soc’y Med. at 298. See also Woodside and Davis, supra, 35 T. 

Jefferson L. Rev. at 119 (“Not only must the exposure precede the development of the 

alleged symptoms, but the period of time between the alleged exposure and the onset of 

symptoms for which compensation is sought must be consistent with the known latency 

period for the exposure in question. The latency period is the period of time between 

exposure to an agent and manifestation of disease symptoms.”). 

5. Biological gradient or dose-response curve of the association. The 

biological gradient factor seeks to show or determine whether increased exposure to a 

chemical agent increases the incidence of the disease. Hill addressed this factor as follows: 

[I]f the association is one which can reveal a biological 

gradient, or dose-response curve, then we should look most 

carefully for such evidence. For instance, the fact that the death 

rate from cancer of the lung rises linearly with the number of 

cigarettes smoked daily, adds a very great deal to the simpler 

evidence that cigarette smokers have a higher death rate than 

non-smokers. That comparison would be weakened, though not 

necessarily destroyed, if it depended upon, say, a heavier death 

rate in light smokers and a lower rate in heavier smokers. We 

should then need to envisage some much more complex 

relationship to satisfythe cause-and-effect hypothesis. The clear 

dose-response curve admits of a simple explanation and 

obviously puts the case in a clearer light. 

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The same would clearly be true of an alleged dust hazard 

in industry. The dustier the environment the greater the 

incidence of disease we would expect to see. Often the 

difficulty is to secure some satisfactory quantitative measure of 

the environment which will permit us to explore this 

dose-response. But we should invariably seek it. 

Hill, supra, 58 Proc. Royal Soc’y Med. at 298. See also King, 762 N.W.2d at 40 (“A 

dose-response relationship is primarily a hallmark of toxicology. If higher exposures to the 

agent increase the incidence of disease, the evidence strongly suggests a causal 

relationship.”). 

6. Plausibility of the causation. Showing that an association is causal is 

easier when biological or other facts support such a conclusion. However, such evidence is 

not essential. Hill tersely commented on this factor as follows: 

It will be helpful if the causation we suspect is 

biologically plausible. But this is a feature I am convinced we 

cannot demand. What is biologically plausible depends upon 

the biological knowledge of the day. 

Hill, supra, 58 Proc. Royal Soc’y Med. at 298. See also King, 762 N.W.2d at 41-42 (“When 

experts know how a disease develops, an association should show biological consistency 

with that knowledge. . . . An expert’s inability to explain a disease’s pathology or 

progression goes to the weight of the evidence, not to its admissibility.”). 

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7. Coherence of the explanation. The viability of an association is enhanced 

when it does not conflict with what is known about the study variables, and when competing 

plausible theories or hypotheses do not exist. In other words, an association should be 

coherent with relevant other knowledge. Hill commented on this factor as follows: 

[T]he cause-and effect interpretation of our data should not 

seriously conflict with the generally known facts of the natural 

history and biology of the disease–in the expression of the 

Advisory Committee to the Surgeon-General it should have 

coherence. 

Thus in the discussion of lung cancer the Committee 

finds its association with cigarette smoking coherent with the 

temporal rise that has taken place in the two variables over the 

last generation and with the sex difference in mortality–features 

that might well apply in an occupational problem. The known 

urban/rural ratio of lung cancer mortality does not detract from 

coherence, nor the restriction of the effect to the lung. 

Hill, supra, 58 Proc. Royal Soc’y Med. at 298. See also Woodside and Davis, supra, 35 T. 

Jefferson L. Rev. at 123 (“The difference between coherence and plausibility would seem, 

in part, to be one of semantics. While plausibility is worded positively (an association should 

be in line with substantive knowledge), coherence is presented negatively (an association 

should not seriously conflict with substantive knowledge). Consideration of coherence 

would reject an observed result as non-causal if it contradicted a predominant theory; while 

plausibility leaves the researcher more room regarding which particular piece of substantive 

knowledge to evaluate the results against.”). 

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8. Experimental data. An association can be enhanced byanyrelated research 

that is based on experiments. Hill said the following about this factor: 

Occasionally it is possible to appeal to experimental, or 

semi-experimental, evidence. For example, because of an 

observed association some preventive action is taken. Does it 

in fact prevent? The dust in the workshop is reduced, 

lubricating oils are changed, persons stop smoking cigarettes. 

Is the frequency of the associated events affected? Here the 

strongest support for the causation hypothesis may be revealed. 

Hill, supra, 58 Proc. Royal Soc’y Med. at 298-99. See also Woodside and Davis, supra, 35 

T. Jefferson L. Rev. at 124 (“From a scientific standpoint, it is unfortunate that this type of 

evidence is generally not available. When an agent’s effects are suspected to be harmful, 

researchers cannot knowingly expose people to the agent. It is difficult to design these types 

of studies due to the ethical implications of experimentation on humans.”). 

9. Existence of analogous causal relationships. This factor seeks to 

determine whether an accepted phenomenon in one area can be applied to another area. Hill 

tersely commented on this issue as follows: 

In some circumstances it would be fair to judge by 

analogy. With the effects of thalidomide and rubella before us 

we would surely be ready to accept slighter but similar evidence 

with another drug or another viral disease in pregnancy. 

Hill, supra, 58 Proc. Royal Soc’y Med. at 299. See also Woodside and Davis, supra, 35 T. 

Jefferson L. Rev. at 125 (“Recent case law has cast caution upon the extent to which 

42
 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

evidence of analogy may be considered in developing opinions on causation. Courts have 

warned that a reliable methodology must still be utilized in drawing analogies.”). 

G. Qualification, Methodology and Opinion of the Expert Witnesses 

As previously mentioned, the three expert witnesses who testified for the 

Petitioner at the evidentiary hearing were Dr. Infante, Dr. Goldstein and Dr. Durie. CSX 

called Dr. Shields and Dr. Green as expert witnesses. In this section we will summarize each 

expert’s qualifications, methodology and opinion. 

1. Dr. Infante’s qualifications, methodology and opinion. Dr. Infante was 

called as an expert witness by Petitioner. Dr. Infante received a Ph.D. in public health from 

the Department of Epidemiology at the University of Michigan in 1973.22 Dr. Infante has 

published approximately 118 peer reviewed articles in scientific journals, the majority of 

which involve epidemiology causation. Dr. Infante’s area of expertise is occupational 

environmental epidemiology. 

22Dr. Infante also received a D.D.S. degree from the College of Dentistry at the 

Ohio State University in 1966. 

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In 1973, Dr. Infante worked as a research associate at the University of 

Michigan and as an epidemiologic consultant for the World Health Organization in 

Washington, D.C. Dr. Infante was employed as an epidemiologist for the Ohio Department 

of Health from 1974-1975. During the period 1975-1978, Dr. Infante worked as an 

epidemiologist for the National Institute for Occupational Safety and Health (“NIOSH”), 

Center for Disease Control, in Cincinnati, Ohio. While working for NIOSH, Dr. Infante 

performed epidemiological studies of workers who were exposed to chemical substances that 

included benezene, pesticides and vinyl chloride. From 1978-2002, Dr. Infante worked for 

the Occupational Safety and Health Administration (“OSHA”), United States Department of 

Labor, in Washington, D.C. While with OSHA, Dr. Infante was employed as the Director 

of the Office of Carcinogen Identification and Classification (“OCIC”) for five years and as 

the Director of the Office of Standards Review (“OSR”) for nineteen years. Dr. Infante’s 

work at OCIC included identifying workplace substances that had the ability to cause cancer 

and classifying them. Dr. Infante’s work at OSR involved evaluating workplace exposure 

to harmful substances and developing occupational exposure limits for substances that were 

causing cancer in the workplace. This research work involved developing standards for toxic 

workplace substances that included asbestos, arsenic, benzene, cadmium, ethylene oxide and 

formaldehyde. From 2002-2011, Dr. Infante was an adjunct professor and lecturer at the 

School of Public Health and Health Service, George Mason University. 

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During his career Dr. Infante has been a consultant or advisor for the World 

Health Organization, National Institute of Environmental Health Sciences, Department of 

Health and Human Services, National Safety Council, National Academy of Sciences, 

National Cancer Institute, Federal Asbestos Taskforce, and the American Public Health 

Association. Dr. Infante is a Fellow in the American College of Epidemiology. 

Dr. Infante was retained in this litigation to render an epidemiological opinion 

as to whether there was an association between diesel exhaust and multiple myeloma, and 

whether diesel exhaust caused Mr. Harris’ multiple myeloma. Dr. Infante relied upon the 

epidemiological methodology in conjunction with the Bradford Hill criteria. 

Dr. Infante reviewed epidemiology literature involving railroad worker diesel 

exhaust exposure and multiple myeloma; animal cancer studies related to diesel exhaust 

exposures; the effects of diesel exhaust on DNA and human lymphocytes; components of 

diesel exhaust that demonstrate an elevated risk of multiple myeloma; and data involving 

exposure to two components of diesel exhaust: pristane and benzene. 

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Dr. Infante testified to reviewing a study by Dr. Tomoko Sonoda et al., 

Meta-Analysis of Multiple Myeloma and Benzene Exposure, 11 J. Epidemiol. 249 (2001),23 

which demonstrated a significant association between engine exhaust and multiple myeloma. 

Dr. Infante testified that the International Agency for Research on Cancer issued Technical 

Publication Number 42 in 2009, and that the publication stated that diesel exhaust exposures 

have been linked to multiple myeloma and leukemia. Dr. Infante further testified that in the 

third edition of a treatise by David Schottenfeld and Joseph F. Fraumeni, Jr., Cancer 

Epidemiology and Prevention, it was reported that studies show an association between 

diesel exhaust and elevated risk of multiple myeloma. 

The report Dr. Infante prepared for the Petitioner summarized the bases for his 

opinion as follows: 

23Dr. Infante defined “meta-analysis” as follows; 

A [meta] analysis is an analysis where you pull the data 

from a number of studies, and you combine the data, and then 

you evaluate the studies that you then select to determine 

whether or not there’s an elevated risk of – of the associations 

that you’re interested in evaluating. 

“Meta-analyses do not involve conducting any new experiments, but are nevertheless highly 

regarded in the scientific community for their ability to synthesize a large amount of data and 

illustrate a general consensus in a particular field.” State v. Lawson, 291 P.3d 673, 700 n.12 

(Or. 2012). 

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Cohort and case-control studies have demonstrated that 

workers exposed to diesel exhaust (DE) have a significantly 

elevated risk of death from [multiple myeloma] MM. 

Epidemiological studies have also demonstrated chromosomal 

damage to B-lymphocytes of workers exposed to diesel exhaust. 

Another cancer of the B-cell line, chronic lymphatic leukemia, 

also demonstrated a significant association with exposure to 

diesel exhaust. Furthermore, benzene, a component of DE, also 

has been significantly associated with an elevated risk of 

developing MM, and pristane, an additional component of DE, 

has demonstrated the induction of plasmacytomas in 

experimental animals. These latter tumors are similar to human 

MM. 

The association between diesel exhaust exposure and 

MM has been derived in the face of several factors that limit the 

ability to detect such an association through epidemiological 

study. The difficulties in identifying an association with MM in 

epidemiological study are a reflection of several factors. . . . In 

spite of the . . . limitations, several cohort studies of workers 

exposed to diesel exhaust now demonstrate elevated risks of 

death from MM . . . . 

Case-control studies which allow for the recruitment of 

much larger cases of MM can be identified in cohort studies also 

have been conducted. A large number of these studies 

demonstrate a significant association between exposure to diesel 

exhaust and MM. 

Diesel exhaust also has been demonstrated to cause DNA 

damage to the lymphocytes of exposed workers. In addition, 

experimental studies demonstrate that diesel exhaust and 

components of diesel exhaust, e.g., polycyclic aromatic 

hydrocarbons, are mutagenic in experimental test systems, and 

cause cancer in experimental animals. Diesel exhaust itself as 

well as additional components of diesel exhaust are known to 

cause cancer in experimental animals, including lymphoma, and 

additional components of DE also demonstrate the induction of 

cancer in experimental animals, including lymphomas. This 

information provides biological plausibility to the 

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epidemiological observations related to diesel exhaust and risk 

of developing MM. 

Ultimately, Dr. Infante opined that there is a significant association between 

diesel exhaust and the risk of multiple myeloma and, that “Mr. Harris’ occupational exposure 

to [diesel exhaust] between 1978 and 2007 were [sic] significant contributing factors and the 

most likely cause of his development of [multiple myeloma].”24 

2. Dr. Goldstein’s qualifications, methodology and opinion. Dr. Goldstein 

was called as an expert witness by Petitioner. Dr. Goldstein received a Ph.D. in biology in 

1962 from the State University of New York, at Buffalo. Dr. Goldstein has published 

roughly 60 peer reviewed articles in scientific journals. Dr. Goldstein’s area of expertise is 

animal toxicology, specifically with respect to polycyclic aromatic hydrocarbons.25 

From 1972 to 1989, Dr. Goldstein worked at the University of California, at 

San Francisco, in various capacities, including associate professor in the Department of 

24During his testimony, Dr. Infante acknowledged that he reviewed literature 

that did not support his opinion. 

25“Polycyclic aromatic hydrocarbons (PAHs) are a group of over 100 different 

chemicals that are formed during the incomplete burning of coal, oil and gas, garbage, or 

other organic substances like tobacco or charbroiled meat. PAHs are usually found as a 

mixture containing two or more of these compounds, such as soot.” Agency for Toxic 

Substances and Disease Registry, 

http://www.atsdr.cdc.gov/substances/toxsubstance.asp?toxid=25 (last visited Nov. 8, 2013). 

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Radiology Oncology. From 1989 to 2002, Dr. Goldstein was employed as a researcher by 

Electric Power Research Institute (“EPRI”), Palo Alto, California. While at EPRI, Dr. 

Goldstein conducted and supervised research involving the toxicological hazards caused by 

polycyclic aromatic hydrocarbons that are found in coal tars.26 The World Health 

Organization employed Dr. Goldstein in 2002 to evaluate and compare radiation hazards 

associated with cell phone use with that of carcinogenic hazards associated with coal tars. 

In 2004, the federal Environmental Protection Agency hired Dr. Goldstein to be part of a 

group that was charged with the responsibility of revising the approach used to evaluate the 

polycyclic aromatic hydrocarbon hazard caused by complex mixtures such as coals. 

Dr. Goldstein was retained in this litigation to render an opinion as to whether 

diesel exhaust caused multiple myeloma. Dr. Goldstein testified that he relied upon the 

weight of the evidence methodology to render his opinion. 

Dr. Goldstein reviewed literature from governmental and international agencies 

that addressed the issue of whether diesel exhaust caused cancer in general. This literature 

included publications from the Environmental Protection Agency,27 International Agency 

26Dr. Goldstein testified that polycyclic aromatic hydrocarbons are found in 

diesel exhaust as well as coal tar. He also testified that “[c]hemically they are the same, but 

their distribution and concentration within the two sources would vary.” 

27The EPA’s published report concluded the following: 

(continued...) 

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for Research on Cancer,28 National Institute of Occupational Science and Health, National 

27(...continued) 

II.A.1. Weight-of-Evidence Characterization 

Using U.S. EPA’s revised draft 1999 Guidelines for Carcinogen 

Risk Assessment (U.S. EPA, 1999), diesel exhaust (DE) is likely 

to be carcinogenic to humans by inhalation from environmental 

exposures. The basis for this conclusion includes the following 

lines of evidence: 

[1] strong but less than sufficient evidence for a causal 

association between DE exposure and increased lung cancer risk 

among workers in varied occupations where exposure to DE 

occurs; 

[2] extensive supporting data including the demonstrated 

mutagenic and/or chromosomal effects of DE and its organic 

constituents, and knowledge of the known mutagenic and/or 

carcinogenic activity of a number of individual organic 

compounds that adhere to the particles and are present in the DE 

gases; 

[3] evidence of carcinogenicity of DPM and the 

associated organic compounds in rats and mice by other routes 

of exposure (dermal, intratracheal, and subcutaneous and 

intraperitoneal injection); and 

[4] suggestive evidence for the bioavailability of DE 

organic compounds from DE in humans and animals. 

Diesel Engine Exhaust (CASRN N.A.) Integrated Risk Info. Syst., U.S. Envtl. Prot. Agency, 

http://epa.gov/IRIS/subst/0642.htm (last visited Nov. 8, 2013). 

28Dr. Goldstein reported data from a 1988 study by IARC, which found diesel 

exhaust “probably carcinogenic to humans (Group 2A).” It appears that after Dr. Goldstein’s 

testimony and report in 2011, IARC released a new study on June 12, 2012, which “classified 

diesel engine exhaust as carcinogenic to humans (Group 1), based on sufficient evidence 

that exposure is associated with an increased risk for lung cancer.” International Agency for 

Research on Cancer, World Health Org., IARC:Diesel Engine Exhaust Carcinogenic, 

(continued...) 

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Toxicology Program of the National Institutes of Environmental Health Science, and the 

American Conference of Certified Industrial Hygienists. Based upon his review and analysis 

of the literature on the subject, Dr. Goldstein opined that diesel exhaust can cause cancer in 

general. 

In determining whether diesel exhaust caused multiple myeloma, Dr. Goldstein 

focused his research on the polycyclic aromatic hydrocarbon chemicals that are found in 

diesel exhaust. After reviewing literature involving animal studies and the effects of 

polycyclic aromatic hydrocarbons, Dr. Goldstein found that polycyclic aromatic hydrocarbon, 

ingested through the lungs and carried through the bloodstream, can travel into bone marrow 

and impact blood forming organs that are responsible for the development of multiple 

myeloma. In other words, Dr. Goldstein opined that polycyclic aromatic hydrocarbons 

caused multiple myeloma.29 

28(...continued) 

http://www.iarc.fr/en/media-centre/pr/2012/pdfs/pr213_E.pdf (last visited on Nov. 8, 2013). 

29Dr. Goldstein made clear that no study that he reviewed stated definitively 

that polycyclic aromatic hydrocarbons caused multiple myeloma. His opinion was based 

upon the weight of the evidence. 

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Dr. Goldstein’s report set out an analysis of the degree to which Mr. Harris was 

exposed to diesel exhaust:30 

In evaluating the risk posed to Mr. Harris by diesel 

exhaust in his work environment it is important to get some idea 

of the dose. Unfortunately no contemporaneous measures of 

relevant contaminants were made in the time before his 

diagnosis. . . . What I will therefore attempt to do is put the dose 

ratio into perspective by using available data (including 

anecdotal evidence) as well as guidelines for diesel exhaust 

proposed by the American Conference of Governmental 

Hygienists for a Threshold Value limit for diesel exhaust of 

0.15mg/m3 (Time Weighted Average). It is intended to provide 

a perspective of the conditions when a train was dragging a full 

load uphill in an unvented tunnel. 

For this calculation I assume that the engines on Mr. 

Harris’ run were 3000 hp and met the exhaust standards of 0.6 

g particulate matter and 1.0 g total hydrocarbons (PAH) per bhphr for diesel engines manufactured between 1973 and 2001 (63 

CFR 18997-19084, 16 Apr. 1998). Thus each locomotive in the 

consist taking 10-20 minutes to pass through one of the longer 

tunnels on the Allegheny and New River routes would have 

produced 300-600 g of particulate matter. Using Stretcher’s 

Neck for this example, the tunnel is 1588 feet long and the bore 

30Courts have 

recognized that in toxic tort cases it is generally 

difficult or impossible to quantify a plaintiff’s 

exposure to a toxin[.] [Therefore], [i]t is not 

always necessary for a plaintiff to quantify 

exposure levels preciselyor use the dose-response 

relationship, provided that whatever methods an 

expert uses to establish causation are generally 

accepted in the scientific community. 

Nonnon v. City of New York, 932 N.Y.S.2d 428, 436-37 (N.Y. App. Div. 2011). 

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is 21' x 25 feet (estimated from photos of the tunnel), the tunnel 

has a volume of 30878 cubic yards. For a roughly 10-20 minute 

exposure the trainmen would have been in an environment of 

9.7-19.5mg/yd3 of particulate matter, though the concentration 

in the engine cab would likely be less. To put this in 

perspective, the ACGLH proposed (subsequently withdrawn) a 

threshold limit of value 0.5-0.15mg/m3 (one m3 and one yd3 are 

essentiallythe same) time weighted average of particulate matter 

for an 8 hour workday in its recommendation. Using the 

0.15mg/m3 value, Mr. Harris found himself surrounded by an 

environment that exceeded the proposed 8 hour average 

concentration limit by 65-to-130-fold. . . . 

. . . . 

It is my opinion that Mr. Harris through his employment 

by CSX was exposed to high levels of diesel exhaust, an agent 

determined by scientific and medical experts to be a probable or 

likely human carcinogen. Absent other factors, it can be 

reasonably concluded that this exposure was a major factor in 

his multiple myeloma. The weight of scientific and medical 

evidence from humans, animal studies, studies with tissues and 

cells using diesel exhaust, closely related pyrogenic materials 

and chemicals known to be in diesel exhaust supports this 

conclusion as does an understanding of the conditions under 

which Mr. Harris worked for 29 years. 

3. Dr. Durie’s qualifications, methodology and opinion. Dr. Durie was 

called as an expert witness by Petitioner. Dr. Durie received a medical degree in 1966 from 

the University of Edinburgh Medical School, Edinburgh, Scotland. Dr. Durie has published 

approximately 400 peer reviewed articles in scientific journals, the majorityof which involve 

multiple myeloma. He has been recognized as one of the top ten multiple myeloma 

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researchers in the world. Dr. Durie is board certified in internal medicine, hematology and 

oncology. 

From 1972-1992, Dr. Durie was on the faculty at the University of Arizona 

College of Medicine. Dr. Durie was on the faculty at Charing Cross and Westminster 

Medical School, University of London, from 1989-1992. From 1993 to the present, Dr. 

Durie has been the Director of Hematologic Research and Myeloma Programs at 

Cedars-Sinai Comprehensive Cancer Center at the University of California, Los Angeles 

(“UCLA”). During his career, Dr. Durie has spent roughly thirty years doing laboratory 

research involving multiple myeloma. Additionally, for many years, Dr. Durie prepared 

summaries of every article that was published on multiple myeloma and presented the 

material at the Annual Review of Medicine. 

Dr. Durie was retained in this litigation to render an opinion as to whether 

diesel exhaust caused multiple myeloma. Dr. Durie testified that he relied upon the Bradford 

Hill methodology to render his opinion. 

Dr. Durie reviewed reports by the Environmental Protection Agency, 

International Agency for Research on Cancer, and National Toxicology Program of the 

National Institutes of Environmental Health Science, which concluded that diesel exhaust 

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contained chemicals that were carcinogenic in humans, such as benzene and polycyclic 

aromatic hydrocarbons. He consulted a report linking diesel exhaust with multiple myeloma 

and epidemiologic literature concerning diesel exhaust and multiple myeloma. He reviewed 

animal studies involving exposure to benzene, polycyclic aromatic hydrocarbons and 

pristane. Dr. Durie reviewed the literature showing that benzene caused the loss of certain 

chromosomes, and that Mr. Harris suffered the same chromosomal damage. Dr. Durie 

testified that during his career, he has treated thousands of patients with multiple myeloma 

and that when he asked “them what their job is, it is amazing how frequently they’ll say 

they’re an engineer or that they’re working with chemicals. And so the occurrence of 

occupations where there is a risk of exposure is remarkably frequent.” 

Dr. Durie’s written report summarized his findings indicating the causal 

relationship of diesel exhaust and multiple myeloma as follows: 

[1] Martyn T. Smith and the group al-Berkley California 

have detailed the chromosomal changes linked to human 

benzene exposure. These chromosome changes include specific 

findings in the bone marrow myeloma cells from Ronald 

Harris. . . . Ronald Harris’s myeloma thus manifests a 

chromosomal pattern characteristic of benzene exposure. 

. . . . 

[2] The linage between diesel exhaust carcinogen 

exposure and the development of multiple myeloma in the case 

of Ronald Harris is thus both plausible and highly probable. 

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[3] Of note the more likely than not association between 

multiple myeloma and diesel exhaust exposure is supported by 

the known presence of multiple other toxic compounds in the 

exhaust [such as the] pristane chemical studied extensively by 

Michael Potter since the 1960’s and known to [have] induced 

plasmacytomata in mice (analogous to human multiple 

myeloma). Recent studies at UCLA have shown that pristane 

levels can be measured in vivo in humans and linked to immune 

regulatory dysfunction with increased B-cell activation. 

Myeloma is derived from abnormal B-lymphocytes. In addition, 

diesel exhaust contained many of the same polycyclic aromatic 

hydrocarbons found in coal tar and pitch blends both of which 

are known human carcinogens. Heavy metals such as nickel are 

also present with known carcinogenic potential. All this 

reinforces the plausible and probable causative relationship 

between diesel exhaust and the development of multiple 

myeloma. 

. . . . 

[4] I strongly support the fact that in the case of Ronald 

Harris the workplace exposures at CSX Transportation Inc. were 

more probably than not a causative factor in the development of 

multiple myeloma. 

4. Dr. Shields’ qualifications, methodology and opinion. Dr. Shields was 

called as an expert witness by CSX. Dr. Shields received a medical degree in 1983 from 

Mount Sinai School of Medicine, New York. Dr. Shields has published approximately 154 

peer reviewed articles in scientific journals. Dr. Shields’ area of expertise includes 

hematology and oncology. Dr. Shields is board certified in internal medicine and oncology. 

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From 1984-1989, Dr. Shields worked as a civilian physician at three medical 

facilities in Washington, D.C. Dr. Shields served as a commissioned officer in the United 

States Public Health Service Commissioned Corps from 1990-199931 and ultimately attained 

the rank of captain. From 2000 to the 2011, Dr. Shields was on the faculty at Georgetown 

University Medical Center. From 2006-2008, Dr. Shields was the senior medical director 

at Capital Breast Care Center in Washington, D.C. During the hearing in this case, Dr. 

Shields testified that he was now employed with the Ohio State University Comprehensive 

Cancer Center. 

Dr. Shields was retained by CSX to render an opinion as to whether diesel 

exhaust caused multiple myeloma. Dr. Shields testified that he relied upon the Bradford Hill 

methodology to render his opinion. 

Dr. Shields testified that he went on the internet to a website run by the 

National Institute of Health and researched articles dealing with diesel exhaust and multiple 

myeloma. Dr. Shields indicated that he reviewed twenty or more papers that involved 

railroad workers and cancers. Dr. Shields testified that he “inferred” from this data that 

31Commissioned Corps officers serve in a variety of positions throughout the 

United States Department of Health and Human Services and certain other federal agencies. 

See United States Pub. Health Serv. Commissioned Corps, U.S. Dep’t. of Health & Human 

Servs., http://www.usphs.gov/aboutus/mission.aspx (last visited on Nov. 8, 2013). 

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myeloma was not found in the studies because it was not mentioned. Specifically, Dr. 

Shields stated that “if myeloma was going to arise from the way they’re describing Mr. 

Harris’ exposure, these studies would show it.” Dr. Shields acknowledged that he was aware 

of a study that showed a significant association between myeloma and railroad workers. Dr. 

Shields discounted the study because, in his opinion, the study did not implicate diesel 

exhaust as a cause for any of the cancers. Several other studies linking myeloma and diesel 

exhaust were found not to be significant by Dr. Shields. Studies that showed an association 

between benzene and myeloma were also rejected by Dr. Shields as not significant to 

establish causation. Ultimately, Dr. Shields opined that, from his review of the literature, 

“there’s no evidence or there’s insufficient evidence that railroad workers are at increased 

risk of myeloma.” At the conclusion of Dr. Shields direct examination, counsel for CSX 

asked the following question: 

Q. Do you have an opinion as to whether the hypothesis 

in this case that exposure to diesel exhaust causes multiple 

myeloma has been proven? 

A. Yes. It’s my opinion that it – that it’s not been proven. 

5. Dr. Green’s qualifications, methodology and opinion. Dr. Green was 

called as an expert witness by CSX. Dr. Green received a Ph.D. in food science and 

technology from the Department of Nutrition and Food Science at Massachusetts Institute 

of Technology in 1981. Dr. Green has published approximately 139 peer reviewed articles 

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in scientific journals. She is also the author of “In Search of Safety: Chemicals and Cancer 

Risk” (Harvard University Press 1988). Dr. Green’s area of expertise is toxicology. Dr. 

Green is a board certified toxicologist. 

Dr. Green was a research director of Scientific Conflict Mapping Project at 

Harvard University from 1983-1985. From 1985-1989, Dr. Green was employed at Meta 

Systems, Inc., as vice president of Environmental Health and Toxicology. From 1989 to the 

present, Dr. Green has been president of Cambridge Environmental, Inc. 

Dr. Green was retained by CSX to render an opinion as to whether diesel 

exhaust caused multiple myeloma. Dr. Green did not indicate any specific methodology that 

she used to render her opinion. However, her testimony suggests she followed the Bradford 

Hill methodology. 

Dr. Green testified that she does not know of any literature linking any type of 

cancer through the inhalation of pristane. Dr. Green also testified that neither the 

Environmental Protection Agency’s Health Assessment Document for Diesel Engine Exhaust 

nor the National Toxicology Program support the assertion that diesel exhaust causes 

myeloma cancer. Dr. Green found a study of Swedish workers by Dr. Paolo Bofetta was 

irrelevant, even though the study showed that over 800 workers exposed to diesel exhaust 

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contracted multiple myeloma. Dr. Green found the study was not significant because over 

800 other men who were studied contracted multiple myeloma, but there was no evidence 

that they also were exposed to diesel exhaust. Dr. Green opined that “diesel engine exhaust 

might cause lung cancer, but there is no credible evidence that it causes multiple myeloma.” 

H. The Circuit Court’s Orders Excluding the
 

Testimony of Petitioner’s Experts
 

We have no hesitancy in finding that the opinions of Petitioner’s three experts 

regarding the causal link between diesel exhaust and multiple myeloma satisfy certain 

requirements of Rule 702. Their opinions would “assist the trier of fact to understand the 

evidence or to determine a fact in issue.” W. Va. R. Evid. 702. All three experts are 

witnesses “qualified as an expert by knowledge, skill, experience, training, or education.” 

Id. Additionally, the testimony of the experts was relevant to issues in the case. W. Va. 

R. Evid. 402. Thus, the question before us is whether the trial court abused its discretion in 

concluding that the reliability prong of Rule 702 was not met. That issue, properly framed, 

is whether Petitioner’s three experts used reliable methodologies in rendering opinions on 

the causation issue linking diesel exhaust with multiple myeloma. As we will explain, below, 

the trial court’s analysis exceeded this narrow issue. Instead, the court in rendering its ruling, 

addressed the jury question: Did Petitioner’s three experts prove causation? Because the 

trial court exceeded the scope of its narrow review of the reliability prong of Rule 702, we 

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find it necessary to examine cases that have demonstrated the narrow focus used to make the 

reliability determination. 

To begin, the court in King v. Burlington Northern Santa Fe Railway Co., 762 

N.W.2d 24 (Neb. 2009), provided an excellent analysis of the limited gatekeeper role of trial 

courts. In King, the wife of a deceased former railroad employee brought an action seeking 

damages against the railroad under the Federal Employers’ Liability Act.32 The plaintiff 

alleged that her husband contracted multiple myeloma due to his exposure to diesel exhaust 

fumes while working for the railroad as a brakeman. The defendant moved the court to 

exclude the plaintiff’s expert. The opinion in King summed up the arguments and the trial 

court’s ruling as follows: 

Differing epidemiological studies supported the experts’ 

deposition testimony. [Plaintiff’s] expert, Dr. Arthur Frank, 

blamed [decedent’s] multiple myeloma on his exposure to diesel 

exhaust. Of course, [defendant’s] expert, Dr. Peter G. Shields, 

disagreed. He believed that the causes were unknown and that 

the majority of epidemiological studies failed to show that diesel 

exhaust can cause multiple myeloma. The district court 

sustained [defendant’s] motion to exclude Frank’s testimony, 

concluding that it failed to pass muster under our 

Daubert/Schafersman framework. It reasoned that his 

methodology was unreliable because the studies he relied on 

failed to conclusively state that exposure to diesel fuel exhaust 

causes multiple myeloma. 

32The plaintiff’s husband was the original plaintiff, but he died during the 

pendency of the litigation. 

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King, 762 N.W.2d at 31. 

After the trial court excluded the plaintiff’s expert witness in King, it granted 

summary judgment to the defendant. The plaintiff appealed to a Nebraska appellate court. 

The appellate court affirmed. The plaintiff then appealed to Nebraska’s Supreme Court. The 

high court in King reversed the ruling of the trial court after concluding that it applied an 

improper standard for reviewing the admissibility of expert testimony. The opinion in King 

outlined the following limited gatekeeper role of trial courts: 

Here, the parties do not dispute Frank’s qualification to 

give expert medical testimony or to interpret epidemiological 

studies. We see the broad issue as whether under our 

Daubert/Schafersman framework, Frank based his opinion on a 

reliable, or scientifically valid, methodology. . . . 

In determining the admissibility of an expert’s opinion, 

the court must focus on the validity of the underlying principles 

and methodology—not the conclusions that they generate. And 

reasonable differences in scientific evaluation should not 

exclude an expert witness’ opinion. The trial court’s role as the 

evidentiary gatekeeper is not intended to replace the adversary 

system but to ensure that an expert, whether basing testimony 

upon professional studies or personal experience, employs in the 

courtroom the same level of intellectual rigor that characterizes 

the practice of an expert in the relevant field. In sum, while the 

trial court acts as the evidentiary gatekeeper, it is not a 

goalkeeper. 

. . . . 

. . . Absent evidence that an expert’s testimony grows out 

of the expert’s own prelitigation research or that an expert’s 

research has been subjected to peer review, experts must show 

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that they reached their opinions by following an accepted 

scientific method or procedure as it is practiced by others in 

their field. 

Epidemiological statistical techniques for testing a 

causation theory have been subject to peer review and are 

generally accepted in the scientific community. The studies 

Frank relied upon were subject to peer review, and the 

researchers did not develop the statistical techniques used in the 

studies for this litigation. . . . Accordingly, the district court 

needed to consider only two issues regarding Frank’s opinion on 

. . . causation. Were the results of the epidemiological studies 

Frank relied on sufficient to support his opinion regarding . . . 

causation? And did he review the scientific literature or data in 

a reliable manner? In other words, did too great an analytical 

gap exist between the data and Frank’s opinion? 

. . . . 

We believe the district court erred in concluding that 

Frank’s causation opinion was unreliable because Frank could 

not point to a study that concludes exposure to diesel exhaust 

causes multiple myeloma. As explained, individual 

epidemiological studies need not draw definitive conclusions on 

causation before experts can conclude that an agent can cause a 

disease. If the expert’s methodology appears otherwise 

consistent with the standards set out above, the court should 

admit the expert’s opinion. But here, the court did not inquire 

into Frank’s methodology. 

King, 762 N.W.2d at 42-49 (internal quotations and citations omitted). 

Another case, though it did not involve multiple myeloma, which illustrates a 

trial court’s limited gatekeeper role is Milward v. Acuity Specialty Products Group, Inc., 639 

F.3d 11 (1st Cir. 2011). In Milward, the plaintiffs, husband and wife, filed an action against 

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manufacturers of products used in refrigerators. The plaintiff husband worked as a 

refrigeration technician. The plaintiffs alleged that the husband contracted acute 

promyelocytic leukemia (“APL”) as a result of exposure to benzene that was contained in the 

defendants’ products. The trial court held a four day hearing to determine whether plaintiff’s 

expert on causation would be allowed to testify that benzene caused APL. The trial court, 

“in a detailed opinion, ruled that ‘Dr. Smith’s proffered testimony that exposure to benzene 

can cause APL lacks sufficient demonstrated scientific reliability to warrant its admission 

under Rule 702.’” Milward, 639 F.3d at 13. The trial court thereafter dismissed the action. 

The First Circuit Court of Appeals reversed after concluding that the trial court exceeded its 

discretion in finding that the opinion of plaintiffs’ expert was wrong. The First Circuit 

outlined the limited role of the trial court in deciding the admissibility of expert testimony: 

[T]rial courts are [not] empowered to determine which of 

several competing scientific theories has the best provenance. 

Daubert does not require that a party who proffers expert 

testimony carry the burden of proving to the judge that the 

expert’s assessment of the situation is correct. The proponent of 

the evidence must show only that the expert’s conclusion has 

been arrived at in a scientifically sound and methodologically 

reliable fashion. The object of Daubert is to make certain that 

an expert, whether basing testimony on professional studies or 

personal experience, employs in the courtroom the same level of 

intellectual rigor that characterizes the practice of an expert in 

the relevant field. 

So long as an expert’s scientific testimony rests upon 

good grounds, based on what is known, it should be tested by 

the adversarial process, rather than excluded for fear that jurors 

will not be able to handle the scientific complexities. Vigorous 

cross-examination, presentation of contrary evidence, and 

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careful instruction on the burden of proof are the traditional and 

appropriate means of attacking shaky but admissible evidence. 

. . . . 

. . . [T]he alleged flaws identified by the court go to the 

weight of Dr. Smith’s opinion, not its admissibility. There is an 

important difference between what is unreliable support and 

what a trier of fact may conclude is insufficient support for an 

expert’s conclusion. 

The court’s analysis repeatedly challenged the factual 

underpinnings of Dr. Smith’s opinion, and took sides on 

questions that are currently the focus of extensive scientific 

research and debate—and on which reasonable scientists can 

clearly disagree. In this, the court overstepped the authorized 

bounds of its role as gatekeeper. The soundness of the factual 

underpinnings of the expert’s analysis and the correctness of the 

expert’s conclusions based on that analysis are factual matters 

to be determined by the trier of fact. When the factual 

underpinning of an expert’s opinion is weak, it is a matter 

affecting the weight and credibilityof the testimony—a question 

to be resolved by the jury. 

. . . . 

. . . The sum of Dr. Smith’s testimony was not merely that 

it is possible, or even biologically plausible, that benzene causes 

APL. Rather, the sum of his testimony was that a weighing of 

the Hill factors, including biological plausibility, supported the 

inference that the association between benzene exposure and 

APL is genuine and causal. 

The record clearly demonstrates that Dr. Smith’s opinion 

was based on an analysis in which he employed the same level 

of intellectual rigor that he employs in his academic work. In 

excluding Dr. Smith’s testimony, the district court did not 

properly apply Daubert and exceeded the scope of its discretion. 

We reverse the district court’s judgment for the defendants and 

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its exclusion of Dr. Smith’s testimony, and we remand for 

proceedings consistent with this opinion. 

Milward, 639 F.3d at 15-26 (internal quotations and citations omitted).. 

In Wagoner v. Exxon Mobil Corp., 813 F. Supp. 2d 771 (E.D. La. 2011), the 

plaintiff, widow and legal representative of decedent, filed a products liability action against 

manufacturers of benzene-containing products alleging that, as a result of the decedent’s 

exposure to benzene, the decedent contracted and died of multiple myeloma. The defendants 

filed motions to exclude plaintiff’s two causation experts. The basis of the motions, and the 

district court’s rejection of the same, were addressed by the court as follows: 

Defendants have raised five arguments with regard to the 

reliability of the testimony of Dr. Butler and Dr. Saux . . . : 1) 

their opinion rests on studies that do not show statistically 

significant findings; 2) their opinion relies on studies that do not 

examine benzene specifically; 3) their opinion rests on studies 

that are not published in peer-reviewed journals and are 

otherwise flawed; 4) their opinion reflects an incomplete review 

of the relevant literature; and 5) their opinion fails to articulate 

a biologically plausible mechanism for benzene to cause 

[multiple myeloma] and thus does not meet the Bradford Hill 

criteria. 

. . . . 

None of the arguments raised by Defendants in support 

of their motions to exclude Dr. Butler and Dr. Saux are 

persuasive. The two individuals are qualified to render an 

opinion . . ., and at least two studies support the notion that there 

is a statistically significant association between benzene and 

[multiple myeloma]. The fact that those studies may be flawed, 

that there are studies that cut against the two doctors’ opinion, 

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and that the doctors could not articulate a biologically plausible 

mechanism for benzene to cause [multiple myeloma] all go to 

the weight of their opinion, and not the question of 

admissibility. . . . Accordingly, the motions to exclude and for 

summary judgment must be denied. 

Wagoner, 813 F. Supp. 2d at 800-05. 

Finally, in Moreland v. Eagle Picher Technologies, 362 S.W.3d 491 

(Mo. Ct. App. 2012), a Missouri appellate court addressed the admissibility of an expert 

opinion under its rules of evidence in the context of a workers’ compensation claim. The 

employee in Moreland alleged that he developed multiple myeloma as a result of years of 

inhalation of chemicals from plastics that his employer produced. The chemicals in the 

plastics included benzene, trichloroethylene, cadmium, nickel, and platinum. The employee 

produced an expert witness at the administrative level who testified that his exposure to 

benzene caused him to develop multiple myeloma. The employer called an expert witness 

who opined that benzene had never been proven to cause multiple myeloma. The ALJ found 

in favor of the employee and awarded him workers’ compensation benefits. An appellate 

court affirmed the award. In doing so, the appellate court in Moreland set out the following 

relevant discussion regarding the employee’s causation expert: 

Dr. Bernard Goldstein (“Dr. Goldstein”), a professor of 

medicine at the University of Pittsburg [sic] Graduate School of 

Public Health and School of Medicine, and also a physician, 

toxicologist, and hematologist, testified on behalf of Moreland. 

Dr. Goldstein testified he had studied benzene toxicity and 

published close to one hundred papers or reviews upon the 

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subject since the 1960s. Dr. Goldstein also specifically 

published and instructed members of the federal judiciary on 

issues concerning toxicology and, in particular, the issue of 

causation and whether chemical agents should be deemed to 

have caused or contributed to the development of multiple 

myeloma. 

Dr. Goldstein testified that benzene was reasonably 

probable to be a cause of multiple myeloma based upon 

epidemiological data, bioassays (experiments on laboratory 

animals), and mechanistic data. Dr. Goldstein testified that 

these sources of information are recognized by the International 

Agency for Research on Cancer and could be applied to 

substantiate that benzene caused multiple myeloma. . . . 

. . . . 

Dr. Goldstein testified that multiple myeloma is an 

identifiable disease and it is reasonably probable that exposure 

to benzene, either by air or dermal absorption, or both, is a 

substantial factor to cause the compounding of cells that lead 

[sic] to multiple myeloma. 

. . . . 

Here, [the employer] specifically argues only that Dr. 

Goldstein’s opinion is not based on medical certainty, and is not 

based on any medical or scientific facts that are reasonably 

relied upon by experts in the field of medical expertise. 

However, . . . Dr. Goldstein extensively explained many of the 

studies which show causation between benzene and multiple 

myeloma. Further, Dr. Goldstein testified that these sources of 

information are recognized by the International Agency for 

Research on Cancer and could be applied to substantiate that 

benzene causes multiple myeloma. Thus, the facts and data on 

which Dr. Goldstein based his opinions are a type reasonably 

relied on by experts in the field. 

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Accordingly, the Commission’s finding that Dr. 

Goldstein’s testimony meets the standard required of expert 

testimonywas supported bycompetent and substantial evidence. 

Moreland, 362 S.W.3d at 500-04 (internal citations omitted).33 

33In the context of an administrative workers’ compensation claim, this Court 

addressed the issue of the reliability of evidence showing a link between benzene exposure 

and a cancer called chronic myelogenous leukemia. In Casdorph v. West Virginia Office 

Insurance Commissioner, 225 W. Va. 94, 690 S.E.2d 102 (2009), the claimant worked as an 

auto mechanic for the State Police for nearly twenty-two years. After the claimant was 

diagnosed with chronic myelogenous leukemia, he filed a claim for workers’ compensation 

benefits. (The claimant died while the case was pending at the administrative level). The 

claimant alleged that his cancer was caused by his exposure to benzene in the workplace. 

During a hearing before an ALJ the claimant provided evidence from several experts, 

including Dr. Infante, who testified that claimant “had ample opportunity for occupational 

exposure to benzene and other solvents contaminated with benzene due to his occupation and 

stated that benzene is the cause of leukemia and CML is a type of leukemia associated with 

benzene exposure.” Casdorph, 225 W. Va. at 102, 690 S.E.2d at 110. The ALJ found that 

the claimant developed chronic myelogenous leukemia from his exposure to benzene and 

therefore ruled the claim was compensable. The Board of Review reversed the decision of 

the ALJ. On appeal, this Court reinstated the ALJ’s decision. We concluded as follows: 

The medical literature and expert and fact witness 

testimony in this case sufficiently established that a causal link 

between the Appellant’s benzene exposure and CML existed. 

Although the Appellees assert that the case studies cited by 

Appellant showing a causal connection between benzene 

exposure and CML have not been able to get peer reviewed 

textbooks to acknowledge and print them as common or 

accepted consensus medical opinion, we find that these case 

studies, although small, are valid studies that have been peer 

reviewed and published. We acknowledge, as Appellees 

contend, that this Court recognized in State v. Leep, 212 W. Va. 

57, 569 S.E.2d 133 (2002) that “whether a scientific theory is 

generally accepted within a scientific community” is a factor 

that must be weighed in determining whether to allow such 

testimony as evidence. However, we must also be reminded that 

(continued...) 

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The foregoing authorities consistently demonstrate the narrow scope of a trial 

court’s consideration of the admissibility of scientific expert testimony: [a] narrow focus that 

our cases have acknowledged, but which far too often has been misunderstood. Therefore, 

we believe it is necessary to carefully and clearly articulate our standard for reviewing the 

reliability prong of the admission of scientific expert testimony. Thus, we make clear, and 

so hold that, when a trial court is called upon to determine the admissibility of scientific 

expert testimony, in deciding the “reliability” prong of admissibility the focus of the trial 

court’s inquiry is limited to determining whether the expert employed a methodology that is 

recognized in the scientific community for rendering an opinion on the subject under 

consideration. If the methodologyis recognized in the scientific community, the court should 

then determine whether the expert correctly applied the methodology to render his or her 

opinion. If these two factors are satisfied, and the testimony has been found to be relevant, 

and the expert is qualified, the expert may testify at trial. 

33(...continued)
 

the Rules of Civil Procedure and the Rules of Evidence do not
 

strictly apply to workers’ compensation claims.
 

Casdorph, 225 W. Va. at 104-05, 690 S.E.2d at 112-13 (footnote added). It is important to 

note that the decision in Casdorph made clear that it was not evaluating the admissibility of 

the expert testimony under the standards of the rules of evidence, because those rules did not 

strictly apply to workers’ compensation litigation. Casdorph is distinguishable from 

Moreland in that regard because Missouri applies its rules of evidence to workers’ 

compensation litigation. 

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We wish to clarify that the standards outlined above are not new principles 

under this Court’s Daubert/Wilt jurisprudence. These principles have always been an 

implicit part of the Daubert/Wilt analysis. Simply put, however, these principles have not 

been clearly understood or followed by trial courts. For instance, this Court made the 

following observations in Wilt: 

We . . . are of the view that, under Rule 702, there is a 

category of expert testimony based on scientific methodology 

that is so longstanding and generally recognized that it may be 

judicially noticed, and, therefore, a trial court need not ascertain 

the basis for its reliability. 

Thus, we believe that Daubert is directed at situations 

where the scientific or technical basis for the expert testimony 

cannot be judicially noticed and a hearing must be held to 

determine its reliability. 

Wilt, 191 W. Va. at 46, 443 S.E.2d at 203. This limitation recognized in Wilt has been lost 

in practice. Litigants invariably have crowded trial court calendars with purported 

Daubert/Wilt evidentiary hearings whenever an expert is called to testify. This was never the 

intent of our Daubert/Wilt analysis. 

In Gentry v. Mangum, 195 W. Va. 512, 466 S.E.2d 171 (1995), Justice 

Cleckley attempted to clarify how Daubert/Wilt was to be applied by “giv[ing] circuit courts 

more guidance from a procedural standpoint in resolving scientific evidence issues.” 

Gentry, 195 W. Va. at 521, 466 S.E.2d at 180. Gentry pointed out in crystal clear terms that, 

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[a]ctually, most scientific validity issues will be resolved 

under judicial notice pursuant to Rule 201. Indeed, most of the 

cases in which expert testimony is offered involve onlyqualified 

experts disagreeing about the interpretation of data that was 

obtained through standard methodologies. Daubert/Wilt is 

unlikely to impact upon those cases. Therefore, circuit courts 

are right to admit or exclude evidence without “reinventing the 

wheel” every time by requiring parties to put on full proof of the 

validity or invalidity of scientific principles. Where judicial 

notice is appropriate, the circuit court should use it. 

Gentry, 195 W. Va. at 522, 466 S.E.2d at 181. In Syllabus point 4 of Gentry, Justice 

Cleckley simplified and reformulated our Daubert/Wilt standard as follows: 

When scientific evidence is proffered, a circuit court in 

its “gatekeeper” role under Daubert v. Merrell Dow 

Pharmaceuticals, Inc., 509 U.S. 579, 113 S. Ct. 2786, 125 

L. Ed. 2d 469 (1993), and Wilt v. Buracker, 191 W. Va. 39, 443 

S.E.2d 196 (1993), cert denied, 511 U.S. 1129, 114 S. Ct. 2137, 

128 L. Ed. 2d 867 (1994), must engage in a two part analysis in 

regard to the expert testimony. First, the circuit court must 

determine whether the expert testimony reflects scientific 

knowledge, whether the findings are derived by scientific 

method, and whether the work product amounts to good science. 

Second, the circuit court must ensure that the scientific 

testimony is relevant to the task at hand. 

195 W. Va. 512, 466 S.E.2d 171. 

Gentry attempted to show that a full blown evedentiary Daubert/Wilt analysis 

was required only for evaluating a new and/or novel scientific methodology. Recognized 

methodologies are the subject of judicial notice. Moreover, this Court explained in Syllabus 

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point four of Mayhorn v. Logan Medical Foundation, 193 W. Va. 42, 454 S.E.2d 87 (1994), 

that 

[p]ursuant to West Virginia Rules of Evidence 702 an 

expert’s opinion is admissible if the basic methodology 

employed by the expert in arriving at his opinion is scientifically 

or technically valid and properly applied. The jury, and not the 

trial judge, determines the weight to be given to the expert’s 

opinion. 

See 2 Franklin D. Cleckley, Louis J. Palmer, Jr. and Robin Jean Davis, Handbook on 

Evidence for West Virginia Lawyers § 702.02[2][c] (5th ed. 2012) (“The [Daubert/Wilt] 

regime contemplates that trial judges will perform a gatekeeping function, determining 

whether the . . . methodology underlying proffered expert testimonyis scientificallyvalid and 

whether that . . . methodology properly can be applied to the facts in issue.”). We note that 

we are not alone in limiting an evidentiary hearing to determine the reliability of experiments 

conducted for litigation and/or novel scientific methodology. See Nonnon v. City of New 

York, 932 N.Y.S.2d 428, 429 (N.Y. App. Div. 2011) (“[W]e [have] determined that 

plaintiffs’ expert evidence did not require that a hearing be held [because] neither the 

deductions of the expert epidemiologists and toxicologists, nor the methodologies employed 

by them, in reaching their conclusions are premised on . . . novel science[.]” (internal 

quotations and citations omitted)). The court in Nonnon observed that 

epidemiology and toxicology are hardly novel sciences, but 

rather, well-established and accepted methodologies. In such a 

case, the focus moves from the general reliability concerns . . . 

to the specific reliability of the procedures followed to generate 

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the evidence proffered and whether they establish a foundation 

for the reception of the evidence at trial. 

Nonnon, 932 N.Y.S.2d at 435. 

In the instant case, the trial court erred by holding a mini-trial to set out and 

resolve issues that were purely matters for jury consideration.34 The three orders excluding 

Petitioner’s three experts set out and resolved an array of disputed factual matters that were 

exclusively grist for the jury and which had no relevancy to the limited role the trial court had 

under the facts of this case. For instance, as noted by Petitioner, the orders found: 

1. If a difference between a case group and control group 

is not statistically significant then there is no difference at all. 

2. It is acceptable scientific practice to interpret as “not 

different” a study that shows an elevated risk that is not 

statistically significant. 

3. There is substantially more benzene in cigarette smoke 

than diesel exhaust. 

4. Benzene is present only in trivial doses in diesel 

exhaust. 

5. The hypothesis that diesel exhaust causes multiple 

myeloma is confounded by the fact that cigarette smoking does 

not. 

34This Court is fully aware that litigants have abused the limited resources of 

our trial judges by demanding full-blown evidentiary hearings in most cases where expert 

testimony is offered. This opinion is intended to make unequivocally clear that the 

admissibility principles under Daubert/Wilt were never intended to allow the abuse that has 

become routine in our trial courts. 

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6. Most epidemiologic studies must be positive for 

purported causal association to be real. 

7. Of forty-seven (47) studies of diesel exposed workers 

only eight (8) purport to be positive. 

9. The epidemiologic literature investigating a causal 

association between railroad employment and multiple myeloma 

is null and not supportive of the subject hypothesis. 

10. There are approximately ten (10) published studies 

investigating [sic] causal link between benzene and multiple 

myeloma. None of them are positive. 

11. The epidemiologic literature regarding PAH exposure 

and multiple myeloma does not support the subject hypothesis. 

12. IARC Technical Publication 42 was not intended to 

make a causation statement but to express a research agenda. 

13. The general causation hypothesis that exposure to 

diesel exhaust causes multiple myeloma has not been proven. 

Clearly, the above findings made by the trial court should never have been 

considered as part of its limited gatekeeper role in this case. All of the above findings 

involve disputed opinions between the experts. They have nothing to do with the reliability 

of the methodologies used by the Petitioner’s experts. In fact, the trial court could have 

resolved the question of the relevancy and reliability of Petitioner’s experts through 

arguments by the parties and without their experts’ testimony. It is undisputed that the 

methodologies employed by Petitioner’s experts are recognized in the scientific community. 

Ironically, CSX’s experts relied upon the same methodologies. There is also no reasonable 

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dispute that Petitioner’s three experts employed the methodologies in a manner consistent 

with how they are employed in the scientific community. The only issue that was in dispute 

was whether Petitioner’s experts were correct in reaching the conclusions they reached. 

Challenging the latter issue is a matter for jury determination.35 

We understand there will be cases where a party seeks to offer a new and novel 

methodology to explain causation, or where a party’s expert performed a specific experiment 

for trial to show causation. In either of those situations, the rigorous prong of the 

Daubert/Wilt gatekeeper analysis is implicated. In stark contrast, the experts in the instant 

case did not offer new or novel methodologies. The epidemiological, toxicological, weight 

of the evidence and Bradford Hill methodologies they used are recognized and highly 

respected in the scientific community. And, as is detailed in this opinion, those experts 

applied the methodologies consistently with the “level of intellectual rigor that characterizes 

the practice of an expert in the relevant field.” Milward, 639 F.3d at 15. 

35This Court is aware that some courts have excluded expert testimony on the 

issue of whether multiple myeloma is caused by diesel exhaust. See Aurand v. Norfolk S. Ry. 

Co., 802 F. Supp. 2d 950 (N.D. Ind. 2011) (excluding plaintiff experts on multiple myeloma); 

Morin v. United States, 534 F. Supp. 2d 1179 (D. Nev. 2005) (same); Castellow v. Chevron 

USA, 97 F. Supp. 2d 780 (S.D. Tex. 2000) (same); Estate of Mitchell v. Gencorp, Inc., 968 

F. Supp. 592 (D. Kan. 1997) (same); Sutera v. Perrier Grp. of Am. Inc., 986 F. Supp. 655 

(D. Mass. 1997) (same); Richardson v. Union Pac. R.R. Co., 386 S.W.3d 77 (Ark . Ct. App. 

2011) (same); Missouri Pac. R.R. Co. v. Navarro, 90 S.W.3d 747 (Tex. Ct. App. 2002) 

(same). The decisions of the courts in those cases are inconsistent with the standards of 

admissibility of scientific expert testimony that are followed in this jurisdiction. 

76
 
 

 

 

 

IV.
 

CONCLUSION
 

We reverse the circuit court’s orders excluding the testimony of Petitioner’s 

three experts. Furthermore, we reverse the order granting summary judgment in favor of 

CSX. Finally, this case is remanded for further proceedings consistent with this opinion. 

Reversed and Remanded. 

77